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Pearson Edexcel International A Level Biology: Skeletal Muscle, Cardiac Control and Adrenaline (YBI11)

Study guide to Edexcel IAL Biology 7.9-7.15: antagonistic muscles, sliding filaments, SAN and AVN, cardiac output, adrenaline, Core Practical 17.

Subject
Biology
Level
A LEVELS
Topic
Skeletal Muscle, Cardiac Control and Adrenaline
Updated

Aligned to Pearson Edexcel A Level Biology (YBI11), Issue 2. Official specification .

Syllabus page (what it covers and how it is assessed): Pearson Edexcel A Level Biology.

Syllabus points this page covers

YBI11

  • 7 Respiration, Muscles and the Internal Environment (whole topic)

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This guide is aligned to the Pearson Edexcel International Advanced Subsidiary/Advanced Level Biology specification (YBI11), Issue 2. It covers statements 7.9 to 7.15 of Topic 7, including Core Practical 17. Topic 7 belongs to the International A2 (IA2) part of the course; Topics 1 to 4 are International AS (IAS). There are no tiers, and every (i), (ii) and (iii) part is covered.

Related pages: the hub for Edexcel A Level Biology, the printable checklist, the revision notes, the practice questions and the exam preparation page. Test yourself with the free diagnostics.

What this unit covers

Statement What you must be able to do
7.9 How muscles, tendons, the skeleton and ligaments interact to enable movement; antagonistic pairs; extensors and flexors
7.10 (i) Structure of a mammalian skeletal muscle fibre; (ii) structural and physiological differences between fast and slow twitch fibres
7.11 Sliding filament theory: actin, myosin, troponin, tropomyosin, calcium ions, ATP and ATPase
7.12 (i) Myogenic cardiac muscle; (ii) SAN, AVN, bundle of His and Purkyne fibres; (iii) ECGs and abnormal rhythms
7.13 (i) Calculate cardiac output; (ii) ventilation and cardiac output changes, heart rate and ventilation rate control, medulla centres
7.14 The role of adrenaline in the fight or flight response
7.15 Core Practical 17: exercise, tidal volume, breathing rate, minute ventilation and oxygen consumption from spirometer traces

7.9 Movement: muscles, tendons, bones and ligaments

Skeletal muscle can only pull, so movement at a joint needs two muscles that pull in opposite directions. These form an antagonistic pair. When one contracts, the other relaxes and is stretched.

  • A flexor contracts to bend a joint and decrease the angle between the bones.
  • An extensor contracts to straighten a joint and increase the angle.
  • A tendon is a tough, inelastic cord of collagen that joins a muscle to a bone, so the pull of the muscle is transmitted to the bone with little loss.
  • A ligament is a tough, slightly elastic band of collagen that joins a bone to another bone and holds the joint together.
  • The skeleton provides rigid levers and the joint acts as the pivot.

At the elbow, the biceps is the flexor and the triceps is the extensor. To raise the forearm, the biceps contracts and pulls on the radius through its tendon while the triceps relaxes. To lower it, the roles reverse.

7.10 Skeletal muscle fibre and fibre types

(i) Structure of a skeletal muscle fibre

A skeletal muscle fibre is a single, long, multinucleate cell. It is bounded by a cell-surface membrane called the sarcolemma, which folds inwards as T tubules. The cytoplasm is the sarcoplasm, containing:

  • Myofibrils, bundles of contractile protein filaments that run the length of the fibre. They give the fibre its striped (striated) appearance.
  • Sarcoplasmic reticulum, a modified endoplasmic reticulum that stores calcium ions and releases them when the fibre is stimulated.
  • Many mitochondria, lying between myofibrils, which supply ATP.

Each myofibril is divided along its length into repeating units called sarcomeres. One sarcomere is the stretch between two neighbouring Z lines. It contains thin filaments (actin, with troponin and tropomyosin) attached to the Z lines, and thick filaments (myosin) in the centre.

Region What you see What it contains
A band Dark band Whole length of the thick filaments, including any overlap with thin filaments
I band Light band Thin filaments only (spans two neighbouring sarcomeres, cut by a Z line)
H zone Lighter area in the middle of the A band Thick filaments only
M line Centre of the sarcomere Where the thick filaments are linked

(ii) Fast and slow twitch fibres

Feature Slow twitch Fast twitch
Contraction Slower, sustained Faster, more powerful
Fatigue Resistant Fatigue quickly
Main ATP source Aerobic respiration Anaerobic glycolysis, with phosphocreatine
Mitochondria Many Fewer
Myoglobin High (red fibres) Low (paler fibres)
Glycogen store and glycolytic enzymes Lower Higher

Myoglobin stores oxygen in the fibre, so slow twitch muscle looks red.

Worked example: sarcomere length from a micrograph

An electron micrograph is at a magnification of ×20 000. A relaxed sarcomere measures 44 mm on the image, and the same sarcomere contracted measures 34 mm. The A band is 1.6 µm long in both states.

  1. Actual length = image length ÷ magnification. Relaxed: 44 mm ÷ 20 000 = 0.0022 mm = 2.2 µm.
  2. Contracted: 34 mm ÷ 20 000 = 0.0017 mm = 1.7 µm.
  3. Percentage shortening = (2.2 − 1.7) ÷ 2.2 × 100 = 22.7% (22.73%).
  4. Total I band length = sarcomere − A band. Relaxed: 2.2 − 1.6 = 0.6 µm. Contracted: 1.7 − 1.6 = 0.1 µm.

The A band stays the same because the filaments do not shorten; the I band and H zone shorten because the filaments slide past each other.

7.11 The sliding filament theory

When a motor neurone stimulates the fibre, an action potential spreads over the sarcolemma and down the T tubules. This opens channels in the sarcoplasmic reticulum and calcium ions (Ca2+) diffuse into the sarcoplasm.

  1. Ca2+ binds to troponin on the thin filament, which changes shape.
  2. This pulls tropomyosin away from the myosin-binding sites on actin, exposing them.
  3. A myosin head, carrying ADP and inorganic phosphate, binds to actin. This forms an actomyosin cross-bridge.
  4. The myosin head tilts, pulling the actin filament towards the centre of the sarcomere (the power stroke). ADP and phosphate are released.
  5. A new ATP molecule binds to the myosin head, which detaches from actin.
  6. ATPase activity of the myosin head hydrolyses ATP to ADP and phosphate. The released energy resets the head to its original angle, ready to bind further along the actin.

This repeats many times each second. The thin filaments slide inwards, the Z lines move closer and the sarcomere shortens. When stimulation stops, calcium ions are pumped back into the sarcoplasmic reticulum and tropomyosin covers the binding sites again.

ATP therefore has two roles: it detaches myosin from actin, and its hydrolysis provides the energy to re-set the head. Returning calcium ions to the store by active transport also uses ATP.

7.12 The heart’s electrical activity

(i) Myogenic

Cardiac muscle is myogenic: it can initiate its own contraction without a nerve impulse arriving. Nerves only alter the rate.

(ii) Coordinating the heartbeat

  1. The sinoatrial node (SAN), a patch of specialised muscle cells in the wall of the right atrium, is the pacemaker. It sets the rhythm by generating regular waves of electrical excitation.
  2. The wave spreads across both atria, which contract together (atrial systole).
  3. A layer of non-conducting fibrous tissue between atria and ventricles stops the wave passing directly to the ventricles.
  4. The wave reaches the atrioventricular node (AVN) in the septum. The AVN delays it briefly, allowing the atria to finish emptying into the ventricles.
  5. The wave passes down the bundle of His, which runs through the septum.
  6. It then spreads along the Purkyne fibres in the walls, from the apex upwards. The ventricles contract from the bottom upwards (ventricular systole), forcing blood towards the arteries.

(iii) ECGs

An electrocardiogram (ECG) records the electrical activity of the heart from the skin surface. In a normal trace the P wave is atrial depolarisation, the QRS complex is ventricular depolarisation and the T wave is ventricular repolarisation. Heart rate = 60 ÷ time between two R waves (in seconds).

Abnormality ECG feature
Tachycardia Rate above 100 beats per minute, R waves close together
Bradycardia Rate below 60 beats per minute, R waves far apart
Atrial fibrillation Irregular spacing; P waves absent or irregular
Ectopic beat An early extra beat, then a pause

Worked example: the R-to-R time on a trace is 0.80 s. Heart rate = 60 ÷ 0.80 = 75 beats per minute (normal).

7.13 Cardiac output, ventilation and their control

(i) Cardiac output

Cardiac output = stroke volume × heart rate. Stroke volume is the volume of blood pumped out by one ventricle in one beat, and equals end-diastolic volume minus end-systolic volume.

Worked example: at rest, end-diastolic volume is 130 cm³ and end-systolic volume is 55 cm³; heart rate is 70 beats per minute.

  1. Stroke volume = 130 − 55 = 75 cm³.
  2. Cardiac output = 75 × 70 = 5250 cm³ per minute = 5.25 dm³ per minute.
  3. In exercise, heart rate is 160 and stroke volume 110 cm³: cardiac output = 17 600 cm³ per minute = 17.6 dm³ per minute.
  4. Percentage increase = (17.6 − 5.25) ÷ 5.25 × 100 = 235%.

Rearranged: cardiac output 4800 cm³ per minute and stroke volume 80 cm³ give heart rate = 4800 ÷ 80 = 60 beats per minute.

(ii) Delivering oxygen and removing carbon dioxide

During exercise, muscles respire faster, so they use more oxygen and release more carbon dioxide. Ventilation and cardiac output both rise, so more oxygen reaches the muscles each minute and more carbon dioxide returns to the lungs. Deeper, faster breathing keeps the gradient steep at the alveoli.

Control of heart rate. The cardiovascular control centre in the medulla oblongata has two regions. Chemoreceptors in the carotid arteries and aorta detect a fall in blood pH (more carbon dioxide). Impulses go to the centre, and the accelerator pathway sends impulses along sympathetic neurones to the SAN, raising heart rate. When blood pH and pressure return to normal, the decelerator pathway sends impulses along the vagus nerve to the SAN, slowing it. Baroreceptors in artery walls detect blood pressure in a similar way.

Control of ventilation rate. The ventilation centre in the medulla receives input from chemoreceptors that detect rising carbon dioxide and falling pH. It sends impulses to the intercostal muscles and diaphragm, increasing the rate and depth of breathing.

7.14 Adrenaline and fight or flight

Adrenaline is a hormone released from the adrenal glands (the medulla) into the blood during stress or danger. It prepares the body for fight or flight:

  • Heart rate and stroke volume increase, raising cardiac output.
  • Ventilation rate and depth increase and the bronchioles dilate.
  • Glycogen in the liver is converted to glucose and released, raising blood glucose for respiration.
  • Arterioles to the skeletal muscles dilate while arterioles to the gut and skin constrict, so more blood reaches the muscles.

Adrenaline binds to receptors on the target cell’s surface membrane and acts through a second messenger inside the cell. As a hormone, its effect starts more slowly but lasts longer than a nerve impulse.

7.15 Core Practical 17: spirometer traces

A spirometer trace records the volume of air moving in and out of the lungs. Soda lime absorbs the carbon dioxide breathed out, so the baseline of the trace slopes downwards as oxygen is used.

  • Tidal volume = the height of one breath (peak to trough) on the trace.
  • Breathing rate = number of breaths ÷ time, in breaths per minute.
  • Respiratory minute ventilation = tidal volume × breathing rate.
  • Oxygen consumption = fall in baseline volume ÷ time.

Worked example: at rest, 6 breaths occur in 30 s, tidal volume is 0.45 dm³ and the baseline falls 0.50 dm³ in 2 min. During exercise, 10 breaths occur in 20 s, tidal volume is 1.9 dm³ and the baseline falls 3.0 dm³ in 2 min.

  1. Rest rate = 6 ÷ 30 × 60 = 12 breaths per minute. Minute ventilation = 0.45 × 12 = 5.4 dm³ per minute. Oxygen use = 0.50 ÷ 2 = 0.25 dm³ per minute.
  2. Exercise rate = 10 ÷ 20 × 60 = 30 breaths per minute. Minute ventilation = 1.9 × 30 = 57.0 dm³ per minute. Oxygen use = 3.0 ÷ 2 = 1.5 dm³ per minute.
  3. Minute ventilation rises about 10.6 times; oxygen consumption rises 6 times.

Common errors

  • Writing that muscles push, or that tendons join bone to bone.
  • Saying the A band shortens in contraction. It does not.
  • Forgetting that ATP is needed to detach myosin from actin.
  • Saying the AVN speeds up the impulse. It delays it.
  • Mixing cm³ and dm³ in cardiac output.

Official syllabus

Pearson Edexcel International Advanced Subsidiary/Advanced Level in Biology (YBI11), Specification, Issue 2, February 2021, Pearson Education Limited. Statements 7.9 to 7.15 of Topic 7, including Core Practical 17.

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