How does the structure of a muscle fibre allow it to shorten and generate force?
The gross and microscopic structure of skeletal muscle, including the ultrastructure of a myofibril and the sarcomere. The sliding filament theory of muscle contraction, including the roles of actin, myosin, calcium ions and ATP. The structure, location and general properties of slow and fast skeletal muscle fibres.
A focused answer to the AQA 3.6 dot point on skeletal muscle. Covers the sarcomere ultrastructure, the sliding filament theory and the roles of actin, myosin, calcium ions and ATP, plus the properties of slow and fast twitch fibres.
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What this dot point is asking
AQA wants you to describe the ultrastructure of the sarcomere, explain the sliding filament theory with the roles of actin, myosin, calcium and ATP, and compare slow and fast twitch fibres.
The answer
Structure of skeletal muscle
A skeletal muscle is made of many muscle fibres, each a long cell with many nuclei (a syncytium) and a shared cytoplasm called the sarcoplasm containing many mitochondria and an extensive sarcoplasmic reticulum (a store of calcium ions). Each fibre contains many myofibrils, the contractile units, arranged in parallel.
Ultrastructure of the sarcomere
A myofibril is divided into repeating units called sarcomeres, which give skeletal muscle its striped (striated) appearance. Within a sarcomere:
- Actin is the thin filament.
- Myosin is the thick filament with protruding heads.
- The A band (dark) is the length of the myosin and stays the same length during contraction.
- The I band (light) contains only actin and shortens during contraction.
- The H zone (centre, only myosin) shortens during contraction.
- The Z line marks the ends of a sarcomere; Z lines move closer together during contraction.
The sliding filament theory
Muscle contraction is explained by the sliding filament theory: the actin and myosin filaments slide past each other, shortening the sarcomere without the filaments themselves changing length. The roles of calcium and ATP are central.
- An action potential arrives at the neuromuscular junction and travels down the T-tubules, causing the sarcoplasmic reticulum to release Ca2+ into the sarcoplasm.
- Ca2+ binds to troponin, changing its shape so that it pulls tropomyosin away from the actin-myosin binding sites on the actin.
- Myosin heads bind to the exposed sites, forming cross-bridges.
- The myosin heads bend (the power stroke), pulling the actin over the myosin and shortening the sarcomere. ADP and phosphate are released from the myosin head.
- ATP binds to the myosin head, causing it to detach from actin.
- ATPase (activated by Ca2+) hydrolyses ATP to ADP and phosphate; the energy released returns the myosin head to its upright position, ready to bind further along the actin.
- The cycle repeats as long as Ca2+ and ATP are present.
When stimulation stops, Ca2+ is actively pumped back into the sarcoplasmic reticulum (using ATP), tropomyosin re-covers the binding sites, cross-bridges can no longer form, and the muscle relaxes.
Slow and fast twitch fibres
Skeletal muscle contains two main fibre types with different properties suited to different activities.
| Property | Slow twitch | Fast twitch |
|---|---|---|
| Contraction | Slow, sustained | Rapid, powerful, short bursts |
| Main respiration | Aerobic | Anaerobic (glycolysis) |
| Mitochondria | Many | Few |
| Myoglobin and capillaries | High (rich blood supply) | Low |
| Glycogen and phosphocreatine | Lower | High store for fast ATP |
| Fatigue | Resists fatigue | Fatigues quickly |
| Typical location | Postural muscles, calf (soleus), endurance athletes | Eye muscles, arms, sprinters |
Slow twitch fibres are adapted for endurance: many mitochondria and a rich capillary supply with myoglobin (an oxygen store) support continuous aerobic respiration. Fast twitch fibres are adapted for short, powerful contractions: they have stores of phosphocreatine to rapidly generate ATP anaerobically, but build up lactate and fatigue quickly.
Examples in context
Example 1. Rigor mortis and the role of ATP. After death, respiration stops and no more ATP is made. Without ATP the myosin heads cannot detach from actin, so the cross-bridges remain locked and the muscles stiffen, a state called rigor mortis. This vividly shows that ATP is required for the myosin head to release from actin during normal contraction and relaxation.
Example 2. Sprinters versus endurance athletes. Muscle biopsies show elite sprinters have a high proportion of fast twitch fibres, giving explosive, powerful contractions over short distances, while elite distance runners have a high proportion of slow twitch fibres for sustained aerobic work. This illustrates how fibre composition matches the demands of an activity.
Try this
Q1. Describe the role of calcium ions in muscle contraction. [3 marks]
- Cue. Released from the sarcoplasmic reticulum; bind to troponin, changing its shape; this moves tropomyosin to expose the actin-myosin binding sites so cross-bridges can form.
Q2. Explain what happens to the I band, H zone and A band of a sarcomere when a muscle contracts. [3 marks]
- Cue. I band shortens; H zone shortens; A band stays the same length; Z lines move closer together.
Q3. Compare slow and fast twitch muscle fibres. [3 marks]
- Cue. Slow twitch: aerobic, many mitochondria, high myoglobin, fatigue-resistant, sustained contraction. Fast twitch: anaerobic, few mitochondria, high glycogen and phosphocreatine, powerful but fatigue quickly.
Exam-style practice questions
Practice questions written in the style of AQA exam questions on this dot point, with worked answer explainers. The year tag is the paper they imitate, not the source.
2017 AQA6 marksDescribe the sliding filament theory of muscle contraction, including the roles of calcium ions and ATP.Show worked answer →
A 6-mark answer needs calcium exposing the binding sites, the cross-bridge cycle, and ATP for the power stroke and detachment.
- An action potential causes Ca2+ to be released from the sarcoplasmic reticulum into the sarcoplasm.
- Ca2+ binds to troponin, changing its shape and moving tropomyosin away from the actin-myosin binding sites.
- Myosin heads bind to actin, forming cross-bridges.
- The myosin heads bend (the power stroke), pulling the actin filaments over the myosin so the sarcomere shortens and ADP and phosphate are released.
- ATP binds to the myosin head, causing it to detach from actin.
- ATP is hydrolysed by ATPase (activated by Ca2+), recocking the myosin head so it can bind again further along; the cycle repeats while Ca2+ is present.
Markers reward Ca2+ exposing binding sites, cross-bridge formation, the power stroke shortening the sarcomere, and ATP for detachment and recocking.
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