Muscle contractionAQA A-Level Biology: Revision notes
Section 1
The sliding filament mechanism
A muscle contracts when actin (thin) and myosin (thick) filaments slide past each other, so each sarcomere gets shorter. The filaments themselves do not shorten.
During contraction the I band and H zone get narrower, the Z lines move closer, and the A band stays the same length.
The myosin filament has projecting heads that act as ATPase enzymes. Actin carries myosin-binding sites, which in resting muscle are covered by the protein tropomyosin.
Section 2
The role of calcium ions
An action potential spreads along the sarcolemma and into the T-tubules, causing the sarcoplasmic reticulum to release calcium ions into the sarcoplasm.
Calcium ions cause tropomyosin to move, exposing the myosin-binding sites on actin. (The role of troponin is not required.)
When stimulation stops, calcium ions are actively transported back into the sarcoplasmic reticulum, tropomyosin covers the sites again and the muscle relaxes.
Section 3
The cross-bridge cycle
- A myosin head carrying ADP and phosphate binds to an exposed site on actin, forming an actinomyosin cross-bridge.
- The head changes angle, pulling the actin filament towards the centre of the sarcomere (the power stroke), and releases ADP and phosphate.
- A new ATP molecule binds to the head, which detaches from actin.
- ATPase on the head hydrolyses ATP to ADP and phosphate; the energy released returns the head to its original position.
- While calcium ions are present, the head binds again further along the actin and the cycle repeats.
ATP is needed to detach the myosin head, not to attach it. Without ATP the muscle locks, as in rigor mortis.
Section 4
The roles of ATP
ATP is used in contraction in three ways:
- Binding to the myosin head so it detaches from actin
- Hydrolysis by ATPase, giving the energy to re-set the head
- Active transport of calcium ions back into the sarcoplasmic reticulum for relaxation
Muscle stores very little ATP, so it must be regenerated continuously by respiration or by phosphocreatine.
Section 5
Phosphocreatine and the supply of ATP
Phosphocreatine (PCr) is a store of phosphate in muscle. It donates its phosphate group to ADP, regenerating ATP very quickly:
PCr + ADP → creatine + ATP
This needs no oxygen, so it supplies ATP immediately at the start of intense exercise. The store is small and runs out within a few seconds. It is replenished during recovery using ATP from aerobic respiration.
Worked example: a muscle uses ATP at 4 mmol kg⁻¹ s⁻¹ and holds 5 mmol kg⁻¹ ATP and 25 mmol kg⁻¹ PCr. Total = 30 mmol kg⁻¹, so the stores last 30 ÷ 4 = 7.5 s before respiration must supply more ATP.
Say that phosphocreatine regenerates ATP by passing a phosphate to ADP; it is not itself the energy source for contraction.
That's the notes covered.
Carry on to the next subtopic.
Exam questions on Muscle contraction
- A biochemist is investigating how protein filaments interact within the sarcomeres of skeletal muscle. She works with isolated myofibrils from a mammal, to which she can add ATP and calcium ions as she chooses.Explain how the movement of myosin heads causes the sarcomere to shorten.2 marks
- Within a few hours of death, the skeletal muscles of an animal become stiff and cannot be stretched (rigor mortis). During life, a resting muscle is soft and its myofibrils are easily stretched. After death, ATP is no longer made in the muscle and calcium ions leak out of the sarcoplasmic reticulum.When stimulation of a living muscle stops, the muscle relaxes. Explain how.2 marks
- In a 100 m sprint, a muscle uses ATP at a rate of 4 mmol kg⁻¹ s⁻¹. At the start of the race the muscle contains an ATP store of 5 mmol kg⁻¹ and a phosphocreatine store of 25 mmol kg⁻¹. One molecule of phosphocreatine can regenerate one molecule of ATP.Calculate for how long the ATP and phosphocreatine stores together could supply the sprint. State what the muscle must rely on after this time.3 marks
Written by the Exaim team, led by Shaun Daswani (Head of Upper Secondary, Improve ME Institute; MSc Financial Mathematics, Imperial College London; BSc, UCL) and Jason Daswani (operational lead, Improve ME Institute; LSE).