• Muscles can only pull, never push — so they work in antagonistic pairs (e.g. bicep/tricep) across joints, connected to bone by tendons.
• A muscle fibre is a giant, multi-nucleated cell-like unit packed with myofibrils (bundles of actin and myosin) and a specialised ER called the sarcoplasmic reticulum that stores calcium ions.
• Muscle contraction = the sliding filament theory. Calcium ions expose myosin-binding sites on actin; myosin heads bind, bend (power stroke), and pull actin inward — repeating over and over using ATP.
• There are two muscle fibre types: fast twitch (powerful, anaerobic, tire quickly) and slow twitch (endurance, aerobic, tire slowly).
• The heart is myogenic — it beats by itself. A wave of excitation travels SAN → atria → AVN → Bundle of His → Purkyne fibres → ventricles.
• Cardiac output = heart rate × stroke volume. ECGs show this electrical activity as P, QRS, and T waves.
• During exercise, the medulla oblongata — via baroreceptors and chemoreceptors — speeds up heart rate and breathing rate using sympathetic (noradrenaline) and parasympathetic (acetylcholine) neurones.
• Adrenaline reinforces this "fight or flight" response, boosting heart rate and redirecting blood to muscles.
• A spirometer measures tidal volume, breathing rate, oxygen consumption, and respiratory minute ventilation — all of which increase with exercise.

Here's the key insight that unlocks this whole topic: a muscle on its own is useless. Muscles can only do one thing — contract and pull. They cannot push. So for a muscle to actually move your body, it needs something rigid to pull against. That's the skeleton's job: it's incompressible, meaning it won't squash or bend when a muscle tugs on it. Muscle + bone together = movement.

Both are strong connective tissue, but they connect completely different things:

• Tendons connect muscle → bone. They're flexible but do NOT stretch — this matters, because if a tendon stretched like elastic, all the force from your muscle contracting would be "wasted" stretching the tendon instead of moving the bone.
• Ligaments connect bone → bone. Their job is to hold the skeleton together at joints, keeping everything in place.

Because a muscle can only pull, muscles almost always work in pairs, positioned on opposite sides of a joint, pulling in opposite directions. This is called antagonistic muscle action. While one muscle contracts to cause movement, its partner must relax and be stretched back out — otherwise it would fight against the movement.

The classic example is your upper arm:

• A muscle that bends a joint when it contracts = a flexor (the bicep, when raising the arm).
• A muscle that straightens a joint when it contracts = an extensor (the tricep, when lowering the arm).

A "muscle fibre" is a strange kind of cell — so strange that biologists don't even like calling it a normal cell. It's technically a highly specialised cell-like unit that contains many nuclei (it's multi-nucleated), which is exactly why we call it a "fibre" rather than a "cell."

Because muscle fibres are unusual, they get their own special vocabulary for parts that are equivalent to normal cell structures:

Some more essential features of the muscle fibre:

• T-tubules (transverse system tubules) are deep tube-like inward folds of the sarcolemma. They run close to the SR and act like an internal wiring system — spreading the electrical impulse quickly and evenly deep into the fibre, so the whole thing contracts at once rather than just the outer edge.
• The sarcoplasm is packed with mitochondria (for aerobic respiration → ATP for contraction) and myofibrils (the actual contractile machinery, made of actin and myosin filaments).
• The membrane of the SR contains protein pumps that actively transport calcium ions into its lumen for storage. This calcium store is what gets released to trigger contraction — you'll see exactly why in the next section.

Each myofibril is built from two types of protein filament, arranged in a very precise repeating pattern:

• Thick filaments — made of myosin
• Thin filaments — made of actin

Where these filaments overlap (or don't) creates a striped appearance under the microscope, which gives us named bands and lines:

Not all muscle fibres are built for the same job. Some are built for a short, explosive burst of power (sprinting away from danger); others are built to keep going for a long time without giving up (walking, standing, migrating). This is the difference between fast and slow twitch fibres.

This is the heart of the whole topic — the actual mechanism of how a muscle contracts at the molecular level. Take your time here; once you understand the sequence, everything else (fatigue, rigor mortis, ATP's role) makes sense automatically.

• Myosin (thick filament): a fibrous protein with a globular head. The fibrous "tail" anchors it into the thick filament, while many myosin molecules line up with their heads all pointing away from the M line — like oars sticking out from a rowing boat, ready to grab hold of something nearby.
• Actin (thin filament): globular proteins that link together into a chain; two chains twist around each other to form one thin filament. Wrapped around this twisted actin structure are two regulatory proteins:
  • Tropomyosin — a fibrous protein that physically blocks the myosin-binding sites on actin when the muscle is at rest.
  • Troponin — attached at regular intervals; it's the "switch" that responds to calcium ions and moves tropomyosin out of the way.

Here's exactly what happens, in order, every single time a muscle contracts:

1. An action potential arrives at the neuromuscular junction (the specialised synapse between a motor neurone and the muscle fibre).
2. Calcium ions are released from the sarcoplasmic reticulum into the sarcoplasm.
3. Calcium ions bind to troponin, causing it to change shape.
4. This shape change pulls tropomyosin out of the way, which exposes the myosin-binding sites on the actin filament.
5. The globular heads of myosin bind to these newly-exposed sites, forming cross-bridges between the two filaments.
6. The myosin heads bend, dragging the actin filament a tiny distance towards the centre of the sarcomere (the M line). This bending motion is called the power stroke.
7. ATP binds to the myosin head. This causes the head to change shape and detach from actin.
8. The enzyme ATPase hydrolyses the ATP into ADP + inorganic phosphate. This releases the energy needed to swing the myosin head back to its original position — this is the recovery stroke.
9. The myosin head is now ready to bind to a new binding site on actin — one that's a little further along, closer to the Z line — and the whole cycle (power stroke → detach → recovery stroke) repeats.
10. Each repeat pulls the actin filament further inward, so the sarcomere shortens and the Z lines are pulled closer together. This keeps happening — as long as calcium is present and ATP is available — until the muscle is fully contracted.

Relaxation: Once nervous stimulation stops, calcium ions are actively transported back into the SR, leaving troponin's binding sites empty. Troponin returns to its original shape, dragging tropomyosin back over the myosin-binding sites on actin. With the binding sites blocked, no cross-bridges can form, no contraction can occur, and the sarcomere lengthens again as the filaments slide back to their relaxed position.

Cardiac muscle is unlike skeletal muscle in one crucial way: it's myogenic, meaning it contracts without any external nerve stimulus — it generates its own rhythm internally, at roughly 60 beats per minute at rest.

The heartbeat isn't random — it's a carefully coordinated wave of electrical excitation that spreads across the heart in a specific sequence, ensuring the atria contract first and the ventricles contract after, from the bottom up (which pushes blood efficiently upward and out into the arteries).

An electrocardiogram (ECG) uses skin electrodes to detect the heart's electrical activity and display it as a wave pattern. Each part of the wave corresponds to a specific electrical event:

Bigger wave = more electrical activity = stronger contraction.

Cardiac output (CO) is the volume of blood pumped by the heart (from one ventricle) per unit time. An average resting adult has a cardiac output of roughly 4.7 dm³ per minute. Fitter individuals tend to have higher cardiac outputs thanks to thicker, stronger ventricular muscle.

This can be rearranged as needed:

• Heart rate = Cardiac output ÷ Stroke volume
• Stroke volume = Cardiac output ÷ Heart rate

Stroke volume is the volume of blood pumped out of the left ventricle during a single cardiac cycle (i.e. the difference between the ventricle's maximum and minimum volume).

During exercise, muscles contract more often and need much more energy. This drives up the rate of aerobic respiration, which means cells need more oxygen delivered and more CO₂ removed. The body responds by increasing both breathing rate/depth and heart rate.

Breathing is controlled by ventilation centres in the medulla oblongata (part of the brainstem): an inspiratory centre (controls breathing in) and an expiratory centre (controls breathing out). These two centres alternate, switching each other on and off:

1. Inspiratory centre sends nerve impulses to the intercostal and diaphragm muscles → they contract → chest volume increases → air pressure in lungs drops below atmospheric → air flows in. At the same time, it inhibits the expiratory centre.
2. As the lungs inflate, stretch receptors in the lungs are stimulated.
3. These stretch receptors send impulses back to the medulla, which inhibits the inspiratory centre.
4. The expiratory centre, no longer inhibited, sends impulses to the intercostal/diaphragm muscles → they relax → chest volume decreases → air pressure rises above atmospheric → air flows out.
5. As the lungs deflate, stretch receptors become inactive, the inspiratory centre is no longer inhibited, and the cycle begins again.

Here's the key chain of cause-and-effect you need to be able to recite for exam questions:

The cardiovascular control centre, also in the medulla oblongata, controls heart rate by adjusting how frequently the SAN fires. It receives information from two types of receptor:

• Baroreceptors (in aortic and carotid bodies) — detect changes in blood pressure
• Chemoreceptors (in the medulla, aortic and carotid bodies) — detect changes in CO₂, O₂, and pH

The medulla then sends impulses along one of two nerve pathways to the SAN, each using a different neurotransmitter:

In situations that cause stress, fear, or excitement, the sympathetic nervous system stimulates the adrenal medulla (part of the adrenal gland, sitting atop each kidney) to release the hormone adrenaline into the bloodstream. This is the "fight or flight" response — the source of the racing heart, dry mouth, and sweating you feel when startled or nervous.

Because adrenaline is a hormone (not a nerve signal), it travels around the whole body in the blood and binds to receptors on various target organs — meaning its effects are widespread and long-lasting compared to a fast, localised nerve impulse.

• It binds directly to receptors on the SAN, increasing the frequency of excitations → heart rate increases → blood delivered to muscle cells faster → more oxygen and glucose reach the muscles → aerobic respiration rate increases → more energy released for the stressful situation.
• It also stimulates the cardiovascular control centre in the medulla oblongata directly, which increases the frequency of sympathetic impulses to the heart — reinforcing and further speeding up the heart rate.
• It causes blood vessels supplying less essential organs (like the digestive system and skin) to constrict, redirecting more blood toward organs actively involved in the fight-or-flight response (like skeletal muscles).
• Blood flow to the brain stays constant regardless of stress level — the brain is too important to ever be short-changed on blood supply.

This practical uses a spirometer to measure how breathing changes before and after exercise. Make sure you know both how the apparatus works and how to read/calculate values from the trace it produces.

• The subject breathes in and out through the spirometer, which is connected to an airtight chamber (often filled with oxygen).
• Soda lime absorbs the CO₂ from exhaled air — this stops CO₂ building up to dangerous, respiratory-distress-causing levels in the rebreathed air.
• As the subject breathes, a trace is drawn on a rotating drum of paper (classic spirometer) or displayed as a digital graph on a computer (electronic spirometer).
• Because CO₂ is continuously removed but not replaced, the total volume of gas in the chamber gradually falls — this steady decrease is used as a direct measure of oxygen consumption.

1. A resting subject breathes into the spirometer for one minute; record results.
2. The subject exercises for two minutes (e.g. on a treadmill) while the spirometer chamber is refilled with oxygen.
3. Immediately after exercising, the subject breathes into the spirometer again for one minute; record results.
4. Compare the "at rest" trace with the "after exercise" trace.

• Breathing rate: count the number of peaks in one minute.
• Tidal volume: average vertical distance between each peak and the trough right before it (i.e. the difference in lung volume between breathing in and breathing out).
• Note: a small amount of air called the residual volume always stays in the lungs and can never be exhaled — this is why the trace never returns all the way to zero.