AQA A-Level Biology (7402)

## Learning Outcomes

- Understand the structure of skeletal muscle from muscle fibre to myofibril to sarcomere
- Identify the roles of actin, myosin, tropomyosin, calcium ions and ATP in contraction
- Explain the sequence from neuromuscular junction stimulation to sarcomere shortening
- Interpret changes in the A band, I band, H zone and Z lines during contraction
- Explain how muscle relaxation occurs
- Apply synoptic links between muscle contraction, respiration and ATP supply
- Avoid common exam errors involving vague terminology and confused structures

## AQA A-Level Biology (7402) Syllabus

For the AQA A-Level Biology (7402), you are expected to understand skeletal muscle contraction as part of how organisms respond to changes in their internal and external environments, with a focus on the following syllabus points:

- Know the structural hierarchy of skeletal muscle, including muscle fibre, myofibril and sarcomere
- Identify the arrangement of actin and myosin filaments within a sarcomere
- Explain the sliding filament theory of muscle contraction
- Understand the roles of calcium ions, tropomyosin and ATP in actin-myosin cross-bridge cycling
- Describe how an action potential at the neuromuscular junction leads to contraction
- Explain how T-tubules and the sarcoplasmic reticulum help spread excitation and release calcium ions
- State what changes, and what does not change, in a sarcomere during contraction
- Explain how relaxation occurs, including the role of acetylcholinesterase and active transport of calcium ions

## Test Your Knowledge

_Attempt these questions before reading this article. If you find some difficult or cannot remember the answers, look more closely at that area during your revision._

1. What is the difference between a muscle fibre, a myofibril and a sarcomere?
2. Why does the A band stay the same length during contraction?
3. How does calcium ion release allow myosin heads to bind to actin?
4. What are the roles of ATP in both contraction and relaxation?
5. How does stimulation at the neuromuscular junction lead to shortening of the sarcomere?

## Introduction

Muscle contraction is a high-value AQA topic because it brings together cell structure, membranes, proteins, transport, enzyme action, respiration and nervous coordination. In Paper 3, it can also appear in unfamiliar contexts, so you need more than a memorised list. You need to understand the sequence of events and why each step is necessary.

![Neuromuscular stimulation, calcium ion release, cross-bridge cycling, and sarcomere shortening during skeletal muscle contraction.](https://static.pastpaperhero.com/images/aqa-a-level-biology-7402-responses-to-environmental-change-muscle-contraction_00.png)

_Action potential transmission initiates acetylcholine signalling, calcium ion mobilisation, actin–myosin interaction, and shortening of the sarcomere._

Skeletal muscles act as **effectors**. They produce movement when stimulated by motor neurones, but they can only pull, not push. That means contraction must be precise, rapid and reversible. The biology behind that depends on the structure of the sarcomere and the controlled interaction of actin and myosin.

> **Key Term: sarcomere**
> The functional unit of contraction in a myofibril, extending from one Z line to the next.

### Structure of skeletal muscle and the sarcomere

Students often lose marks because they confuse the levels of organisation. A **muscle fibre** is a single long multinucleate skeletal muscle cell. Inside it are many **myofibrils**, and each myofibril is made of repeating **sarcomeres**.

This hierarchy matters because exam questions may ask about changes at one level but expect explanation at another. For example, a whole muscle shortens because many muscle fibres shorten, and each fibre shortens because many sarcomeres shorten at the same time.

> **Key Term: muscle fibre**
> A single long multinucleate skeletal muscle cell containing many myofibrils.
>
> **Key Term: myofibril**
> A long cylindrical contractile structure inside a muscle fibre, made of repeating sarcomeres.

Within each sarcomere, the two main protein filaments are arranged in a very specific way:

- **Actin** forms the thin filaments
- **Myosin** forms the thick filaments with projecting heads
- Actin filaments are attached to the **Z lines**
- Myosin filaments lie in the centre of the sarcomere

If viewed with an electron microscope, this arrangement produces a banding pattern:

- **I band** = actin only
- **A band** = length of the myosin filaments, including overlap with actin
- **H zone** = myosin only, in the middle of the A band
- **Z line** = boundary between sarcomeres
  > **Key Term: A band**
  > The dark band of a sarcomere containing the full length of the myosin filaments, including any overlap with actin.

A common mistake is to say the A band is the overlap region. That is not precise enough. The A band includes the overlap region, but it is defined by the full length of the myosin filaments. This is why it stays the same length during contraction.

The visible changes during contraction provide evidence for the sliding filament theory:

- Z lines move closer together
- I band becomes narrower
- H zone becomes narrower and may disappear
- A band stays the same width

This pattern shows that the filaments themselves do not shorten. Instead, they slide past one another, increasing overlap.

> **Key Term: sliding filament theory**
> The theory that muscle contracts because actin and myosin filaments slide past each other, causing sarcomeres to shorten without the filaments themselves shortening.

Why does this matter? Because examiners often ask for evidence. If the filaments were shortening, the A band would decrease in width. Since it does not, the correct conclusion is that myosin filament length stays constant while actin is pulled inward.

T-tubules and the sarcoplasmic reticulum are also part of the structural setup for contraction. T-tubules are inward folds of the sarcolemma that carry depolarisation deep into the muscle fibre. The sarcoplasmic reticulum stores calcium ions ready for rapid release.

> **Key Term: T-tubules**
> Inward folds of the sarcolemma that conduct depolarisation into the muscle fibre so all parts of the fibre are stimulated quickly.

Muscle fibres contain many mitochondria because contraction needs large amounts of ATP. This links directly to respiration. ATP is needed not just for the power stroke cycle, but also for detachment of myosin and pumping calcium ions back into storage during relaxation.

> **Test Tip:** If a question asks for evidence for the sliding filament theory, do not just describe the cross-bridge cycle. Use sarcomere observations: I band decreases, H zone decreases, Z lines move closer, and A band stays the same.

### From nerve impulse to cross-bridge formation

Muscle contraction starts before actin and myosin interact. It begins at the **neuromuscular junction**, where a motor neurone meets a muscle fibre.

An action potential arrives at the presynaptic terminal of the motor neurone. This causes calcium ion channels in the synaptic knob to open, and calcium ions enter. The calcium ions cause synaptic vesicles to fuse with the presynaptic membrane, releasing **acetylcholine** into the synaptic cleft.

Acetylcholine diffuses across the cleft and binds to receptors on the motor end plate, which is part of the sarcolemma of the muscle fibre. Sodium ion channels open, sodium ions enter, and the sarcolemma depolarises. If threshold is reached, an action potential spreads across the sarcolemma and down the T-tubules.

> **Key Term: neuromuscular junction**
> The synapse between a motor neurone and a skeletal muscle fibre.

The action potential travelling down the T-tubules causes the sarcoplasmic reticulum to release calcium ions into the sarcoplasm. In a relaxed muscle, tropomyosin blocks the binding sites on actin, so myosin heads cannot attach.

When calcium ion concentration rises, calcium ions bind to an associated regulatory protein and this leads to a change in the position of tropomyosin. The binding sites on actin are exposed. Myosin heads can then attach, forming cross-bridges.

> **Key Term: tropomyosin**
> A protein associated with actin that blocks myosin-binding sites when the muscle is relaxed.

This is a good example of how protein shape controls function. The contraction does not start simply because calcium ions are present. It starts because calcium ions alter the arrangement of proteins on the actin filament, exposing the binding sites.

Examiners also expect precision here. At the neuromuscular junction, use **receptor** for acetylcholine on the motor end plate. In the sarcomere, use **binding site** for myosin on actin. Mixing these up can cost marks.

### The cross-bridge cycle, ATP use and relaxation

Once the actin binding sites are exposed, the myosin head attaches to actin to form an actin-myosin cross-bridge. The myosin head then changes angle and pulls the actin filament toward the centre of the sarcomere. This is the power stroke.

As this happens across many myosin heads and many sarcomeres at the same time, the actin filaments are pulled inward from both ends of the sarcomere. The result is shortening of the sarcomere and therefore shortening of the muscle fibre.

ATP is essential at several steps, and students often give only one role. You need the full picture:

- ATP binds to the myosin head, causing it to detach from actin
- ATP is hydrolysed to ADP and inorganic phosphate, releasing energy
- This energy re-cocks the myosin head so it can bind further along the actin filament
- ATP is also used for active transport of calcium ions back into the sarcoplasmic reticulum during relaxation
  > **Key Term: actin-myosin cross-bridge**
  > The temporary attachment formed when a myosin head binds to a binding site on actin.

A clear cycle is:

1. Binding sites on actin are exposed
2. Myosin head binds to actin
3. Myosin head changes angle and pulls actin
4. ADP is released
5. ATP binds to myosin, causing detachment
6. ATP is hydrolysed, re-energising the myosin head
7. The head reattaches further along actin
8. The cycle repeats while calcium ions and ATP remain available

The cycle can happen repeatedly and rapidly, producing smooth contraction rather than a single jerk.

Relaxation is not just “contraction stopping”. It is an active process. When stimulation ends, acetylcholine is hydrolysed by acetylcholinesterase in the synaptic cleft. This prevents continued depolarisation of the sarcolemma.

At the same time, calcium ions are actively transported from the sarcoplasm back into the sarcoplasmic reticulum using ATP. As calcium ion concentration in the sarcoplasm falls, tropomyosin returns to its blocking position over the actin binding sites. Cross-bridge formation stops, and the muscle relaxes.

> **Key Term: sarcoplasmic reticulum**
> Specialised endoplasmic reticulum in muscle fibres that stores and releases calcium ions.

The need for ATP in relaxation is a frequent exam point. Without ATP, myosin cannot detach and calcium ions cannot be pumped back into the sarcoplasmic reticulum. So ATP is needed for both contraction and relaxation.

> **Test Tip:** In 5- or 6-mark questions, organise your answer as a sequence: neuromuscular junction, sarcolemma and T-tubules, calcium ion release, tropomyosin movement, cross-bridge cycle, then relaxation. This keeps your answer logical and prevents missed steps.

### Synoptic links, fibre types and common exam traps

This topic is highly synoptic because contraction depends on energy supply. Muscle fibres contain many mitochondria to generate ATP by aerobic respiration. During intense exercise, ATP demand rises sharply. If oxygen delivery cannot keep up, anaerobic respiration contributes more, and lactate may accumulate.

Phosphocreatine is also useful as a rapid reserve. It cannot power contraction directly, but it can quickly donate phosphate to ADP to regenerate ATP. This is especially useful in short bursts of intense activity.

There are also two main types of skeletal muscle fibre.

**Slow-twitch fibres** contract more slowly and with less force, but they can keep working for longer. They are adapted for endurance by having:

- many mitochondria
- a good blood supply
- lots of myoglobin for oxygen storage

**Fast-twitch fibres** contract quickly and powerfully, but fatigue more rapidly. They are adapted for short, intense activity by having:

- more and thicker myosin filaments
- high glycogen content
- many enzymes for anaerobic respiration
- stores of phosphocreatine

These features explain why different muscles, and different athletes, are suited to different tasks. A marathon runner benefits from many slow-twitch fibres, while a sprinter or weightlifter benefits from more fast-twitch fibres.

Common exam traps include:

- saying actin and myosin filaments contract instead of slide
- saying the A band shortens
- confusing myofibril with muscle fibre
- writing only about the sarcomere when the question asks how contraction is initiated
- forgetting acetylcholinesterase in relaxation
- forgetting ATP is needed to pump calcium ions back into the sarcoplasmic reticulum

A good biological explanation always links structure to function. T-tubules matter because they spread depolarisation deep into the fibre quickly. The sarcoplasmic reticulum matters because calcium must be released rapidly and then removed rapidly. Myosin heads matter because their shape allows repeated attachment, movement and detachment.

## Key Point Checklist

_This article has covered the following key knowledge points:_

- A muscle fibre is a single multinucleate cell containing many myofibrils
- A sarcomere is the functional contractile unit between two Z lines
- Actin forms thin filaments and myosin forms thick filaments with projecting heads
- The I band contains actin only, the H zone contains myosin only, and the A band corresponds to the length of the myosin filaments
- During contraction, Z lines move closer together, the I band narrows and the H zone narrows, but the A band stays the same
- The sliding filament theory states that actin and myosin filaments slide past one another rather than shortening
- At the neuromuscular junction, acetylcholine binds to receptors on the motor end plate and causes depolarisation
- T-tubules carry depolarisation into the muscle fibre and trigger calcium ion release from the sarcoplasmic reticulum
- Calcium ions move tropomyosin away from binding sites on actin so myosin heads can form cross-bridges
- ATP is needed to detach myosin from actin, re-cock the myosin head and actively transport calcium ions back into the sarcoplasmic reticulum
- Acetylcholinesterase breaks down acetylcholine to stop continued stimulation
- Muscle fibres contain many mitochondria because contraction and relaxation require large amounts of ATP

## Key Terms and Concepts

- sarcomere
- muscle fibre
- myofibril
- A band
- sliding filament theory
- T-tubules
- neuromuscular junction
- tropomyosin
- actin-myosin cross-bridge
- sarcoplasmic reticulum


Responses to environmental change - Muscle contraction