Muscle Contraction: MDCAT Biology notes
Muscle contraction MDCAT notes: sliding filament theory, calcium, troponin and tropomyosin, cross-bridge cycle, ATP use, band changes, fatigue, tetany.
Sliding filament theory
A muscle shortens because thin actin filaments slide over thick myosin filaments toward the centre of each sarcomere. The filaments themselves do not get shorter. What shortens is the sarcomere, and with it the muscle fibre.
| Region | During contraction |
|---|---|
| I band | Shortens |
| H zone | Narrows or disappears |
| Z lines | Move closer together |
| Sarcomere | Shortens |
| A band | Stays the same length, because it equals the length of the myosin filaments |
Why a relaxed muscle stays relaxed
In resting muscle, tropomyosin lies along the actin filament and blocks the myosin-binding sites. Troponin holds tropomyosin in this blocking position. $\mathrm{Ca^{2+}}$ is locked away in the sarcoplasmic reticulum.
Sequence of contraction
- A nerve impulse reaches the neuromuscular junction, and acetylcholine depolarizes the sarcolemma.
- The action potential spreads along the sarcolemma and down the T-tubules.
- The first event inside the fibre is that the sarcoplasmic reticulum releases $\mathrm{Ca^{2+}}$ into the sarcoplasm. Calcium is the regulator of contraction.
- $\mathrm{Ca^{2+}}$ binds to troponin. Troponin changes shape and pulls tropomyosin away, which exposes the binding sites on actin.
- Energized myosin heads attach to actin and form cross-bridges.
- Power stroke: the myosin heads pivot and pull actin toward the M line.
- A new ATP binds to the myosin head, and the cross-bridge breaks. The ATP is hydrolysed (ATP → ADP + Pi), which re-cocks the head for another cycle.
- The cycle repeats as long as $\mathrm{Ca^{2+}}$ and ATP are present.
Relaxation
When stimulation stops, $\mathrm{Ca^{2+}}$ is actively pumped back into the sarcoplasmic reticulum, which uses ATP. Tropomyosin covers the binding sites again, cross-bridges can no longer form, and the muscle relaxes.
Role of ATP
- ATP is needed to break (detach) cross-bridges. Without ATP, myosin stays locked to actin. This is why muscles stiffen after death (rigor mortis).
- Its hydrolysis provides the energy for the next power stroke.
- ATP also powers the calcium pump during relaxation.
- Creatine phosphate is the muscle's immediate energy store. It quickly regenerates ATP from ADP.
Fatigue, cramps and tetany
- Muscle fatigue: during heavy exercise, oxygen runs short and anaerobic respiration produces lactic acid. Its accumulation causes tiredness, pain and eventually an inability to contract. The extra oxygen needed later to clear lactic acid is the oxygen debt.
- Tetany: sustained, involuntary spasms caused by low blood $\mathrm{Ca^{2+}}$. It often follows underactivity of the parathyroid glands, since parathormone normally raises blood calcium.
- Cramps are sudden, painful involuntary contractions.
Worked example
Question: A drug stops the calcium pump of the sarcoplasmic reticulum. What happens to the muscle?
Answer: $\mathrm{Ca^{2+}}$ stays in the sarcoplasm, the binding sites stay exposed, and the muscle cannot relax properly.
Common MDCAT traps
- $\mathrm{Ca^{2+}}$ binds troponin, not tropomyosin. Tropomyosin is the blocker.
- The A band does not shorten; the I band and H zone do.
- ATP is used mainly to break cross-bridges and re-cock the myosin head.
- The first event after the impulse is calcium release, not cross-bridge formation.
- Actin and myosin filaments keep their length; the sarcomere shortens.
Quick revision
- Tropomyosin blocks myosin binding sites at rest.
- Calcium is released from the SR and pumped back into it on relaxation.
- ATP is hydrolysed to break cross-bridges.
- Tetany is caused by low blood calcium.
- Lactic acid build-up causes muscle fatigue.