Run For Your Life Flashcards

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1
Q

Describe how joints work.

A

Muscle pairs are antagonistic. Muscles causing extension are extensors and flexors reverse the change.

Tendons join muscle to bone.
Ligaments join bone to bone and are strong and flexible.
Cartilage absorbs synovial fluid and shock.

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2
Q

What makes up muscle cells?

A

Muscles are made up of muscle fibre cells. Muscle fibre cells are multinucleate. These are bound by connective tissues. These make up muscle cells. Muscle cells contain organelles and microfibrils. Microfibrils are made up of sarcomeres.

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3
Q

Describe sliding filament theory.

A

Nerve impulses at a neuromuscular junction release Ca2+ ions from the sarcoplasmic reticulum. These diffuse through the sarcomere. Ca2+ ions attach to troponin on the actin causing tropomyosin to shift position and expose myosin binding sites. Myosin heads bind with binding sites and form cross bridges. This releases ADP and Pi. Myosin changes shape and the myosin head moves forward. Actin moves over the myosin.
ATP binds to myosin causing the head to detach. ATPase hydrolyses ATP to ADP and Pi changing the shape of the myosin head and returning the myosin head to it’s previous position.

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4
Q

Describe glycolysis.

A

Occurs in the cytoplasm. 2x ATP phosphorylate glucose, producing 2x ADP. Glucose splits to form 2x triose phosphate (3C). This is oxidised by 2x NAD to form 2x pyruvate. Phosphate phosphorylates 4x ADP to 4x ATP. There is a net gain of 2x ATP.

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5
Q

Describe the link reaction.

A

Pyruvate is actively transported to the mitochondria. Decarboxylation and dehydrogenation occur, producing 2x 2C molecules. Hydrogen forms reduced NAD. CoenzymeA is added to the 2C compound, along with fatty acids, producing AcetylCoA.

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6
Q

Describe the Krebs cycle.

A

Occurs in the matrix of the mitrochrondia. AcetylCoA combined with a 4C sugar to produce 6C citric acid. Citric acid is oxidised, 3x NAD and 1x FAD are reduced. This forms a 5C sugar. 2x CO2 is removed, producing a 4C sugar. ADP is phosphorylated producing 1x ATP.

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7
Q

Describe the electron transport chain.

A

H+ and e- from glycolysis reduce and oxidise NAD in a cycle. The e- is used in the electron transport chain. The cristae of the mitochondria make ATP in oxidative phosphorylation. FADH produces 1.5x ATP, NADH produces 2.5x ATP. Electrons pass on via redox reactions. Chemiosmosis occurs due to a high concentration of H+ ions. The H+ ions diffuse, allowing ATPase to synthesisr ATP. e-, H+ and oxygen form water.
Loss of oxygen stops transport chain.

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8
Q

Describe anaerobic respiration.

A

In glycolysis, pyruvate is oxidised to produce lactate in animals and ethanol in plants and microorganisms.

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9
Q

Describe the use of creatine phosphate.

A

Stored in muscles and hydrolysed quickly to produce ATP.

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10
Q

Define aerobic capacity.

A

Ability to take in, transport and use oxygen.

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11
Q

Describe VO2.

A

VO2(max) is the maximum amount of oxygen consumption. Measured in ml min-1 kg-1.

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12
Q

How is adequate oxygen supply maintained?

A

Increased cardiac output, faster and deeper breathing rate.

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13
Q

Define cardiac output.

A

Volume of blood pumped by the heart in one minute.

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14
Q

What is the calculation for cardiac output?

A

Cardiac output = stroke volume X heart rate.

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15
Q

Define stroke volume.

A

The volume of blood pumped out of the left ventricle.

During exercise, more blood returns in venous return.

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16
Q

Describe how heart rate is controlled.

A

Heart muscle is myogenic and thus can contract without external nervous stimulation.

Depolarisation starts at the sinoatrial node in the right atrial wall. This generates an electrical impulses which contracts the atria. This impulse delays, allowing the ventricles to fill, before reaching the atrioventricular node. The impulse continues to the Purkinje fibres and then the bundle of His. The ventricles are depolarised and contract.

17
Q

Define tachycardia.

A

Abnormally fast heartbeat. Little blood is pumped, no time to fill.

18
Q

How is tachycardia treated?

A

Relaxation therapy.

Beta blockers.

19
Q

Define bradycardia.

A

Abnormally slow heartbeat. May be caused by good aerobic fitness. Affected by beta blockers and tranquilisers.

20
Q

How does the nervous system control the heart?

A

The autonomic system consists of the accelerator (sympathetic) and the vagus nerve (parasympathetic). The accelerator increases heart rate. Adrenaline dilates arteries, increasing blood flow. The vagus nerve decreases heart rate.
An excessive rise in blood pressure is avoided by negative feedback.

21
Q

Define tidal volume.

A

In and out in each breath.

22
Q

What is the calculation for minute ventilation?

A

Minute ventilation = tidal volume x number of breaths.

23
Q

Describe inhalation.

A

Intercostal and diaphragm muscles contract. Volume increases, ribs move up, diaphragm moves down, low pressure.

24
Q

Describe exhalation.

A

Stretch receptors are stimulated and send inhibitory impulses. Causes elastic recoil. Internal intercostal muscles contract. Volume decreases, ribs move down, diaphragm moves up, high pressure.

25
Q

How is breathing rate controlled?

A

Carbon dioxide dissolves in blood, forming carbonic acid. Dissociates into H+ and HCO3-, lowering pH.
Chemoreceptors in the medulla oblongata detect a change in H+ concentration. Impulses stimulate muscles.

26
Q

Describe the impact the exercise has on breathing rate.

A

Impulses from motor cortex increase ventilation. Impulses from stretch receptors.

27
Q

Describe slow twitch muscle fibres.

A

Many mitochondria, myoglobin (red), capillaries. Fatigue-resistant.

28
Q

Describe fast twitch muscle fibres.

A

White, many sarcoplasmic reticulum, high glycogen content. Fatigues quickly.

29
Q

Define homeostasis.

A

Maintenance of a stable internal environment regardless of external influences.

30
Q

Describe how homeostasis is maintained.

A

Receptors detect a deviation and control effectors in negative feedback.

31
Q

What changes are made when the thermoregulatory centre detects the body is cold?

A

Arteries constrict. Hairs stand on end. Goosebumps. Shivering. Raised metabolic rate.

32
Q

What changes are made when the thermoregulatory centre detects the body is hot?

A

Stimulated sweat glands. Dilated arteries.

33
Q

Describe the effect of over-exercising.

A

Suppresses the immune system. Damage to joints, cartilage damage, tendonitis, bursitis (fluid sacs).

34
Q

How are the effects of over-exercising dealt with?

A

Arthroscopy, keyhole surgery.

Prosthetics.

35
Q

Describe the effect of peptide hormones.

A

Bind to receptors which activate a second messenger, causing chemical change.

36
Q

Describe the effect of steroid hormones.

A

Bind to a receptor, function as a transcription factor, turning on/off enzyme synthesis.

37
Q

Describe the effect of EPO.

A

Peptide hormone, produced by kidneys, forms new blood cells.

38
Q

Describe the effect of testosterone.

A

Steroid hormone, binds to androgen receptors, modifying gene expression, increasing muscle size and strength.

39
Q

Describe the effect of creatine.

A

Not banned. Increases levels of creatine phosphate which produces ATP, improving performance levels.