Question
During muscle contraction, which of the following correctly describes the sequence of events after a nerve impulse reaches the neuromuscular junction?
(A) Ca²⁺ released → troponin binds Ca²⁺ → tropomyosin moves → actin-myosin cross-bridge forms → ATP hydrolysis → power stroke
(B) ATP hydrolysis → Ca²⁺ released → troponin binds Ca²⁺ → cross-bridge forms → power stroke → tropomyosin resets
(C) Troponin moves → Ca²⁺ binds tropomyosin → myosin head activates → power stroke → ATP detaches myosin
(D) Ca²⁺ released → myosin directly binds actin → ATP synthesised → power stroke → troponin resets
Correct Answer: (A)
Solution — Step by Step
When an action potential arrives at the motor end plate, acetylcholine is released. This depolarises the sarcolemma, and the signal travels into the T-tubules, which triggers the sarcoplasmic reticulum to flood the sarcoplasm with Ca²⁺ ions.
This is the initiating event — without Ca²⁺, the whole contractile machinery stays locked.
In the resting state, tropomyosin sits over the myosin-binding sites on actin, physically blocking attachment. Troponin is the calcium sensor — it’s a complex of three subunits (TnC, TnI, TnT), and Ca²⁺ binds specifically to TnC.
This binding causes a conformational change that drags tropomyosin away from the active sites on actin.
With the active sites on actin now exposed, the energised myosin head (already cocked by ATP hydrolysis in the previous cycle, carrying ADP + Pᵢ) attaches to actin. This forms the actin-myosin cross-bridge.
The myosin head is like a cocked gun — the energy from ATP hydrolysis was used to cock it, not to fire it.
Release of inorganic phosphate (Pᵢ) triggers the power stroke: the myosin head pivots, pulling the actin filament toward the M-line. This is what shortens the sarcomere.
ADP is released at the end of the power stroke. The head is now in its “rigor” state — tightly bound, low-energy configuration.
A fresh ATP molecule binds to the myosin head, causing it to detach from actin. ATP is then hydrolysed (by myosin ATPase) to ADP + Pᵢ, which re-cocks the head into the high-energy position, ready for the next cycle.
If ATP runs out (as in rigor mortis), the heads stay locked to actin permanently — which is why the body becomes rigid.
Why This Works
The sliding filament theory (Huxley & Hanson, 1954) tells us that the actin and myosin filaments themselves don’t shorten — the sarcomere shortens because actin slides over myosin toward the centre. The H-zone and I-band narrow; the A-band length stays constant. This distinction appears repeatedly in NEET MCQs.
The reason Ca²⁺ acts as the switch is elegant: tropomyosin is a gatekeeper that prevents wasteful contraction at rest. Troponin-C has a higher affinity for Ca²⁺ than Mg²⁺ at physiological concentrations, so when Ca²⁺ floods in, it selectively triggers the system.
ATP plays two separate roles here — detaching myosin AND providing energy (via hydrolysis) to re-cock the head. Students who treat ATP as “just the energy source” miss the detachment role, which leads to errors on NEET questions about rigor mortis.
Alternative Method — Tracing It via Sarcomere Changes
If the MCQ gives you structural changes instead of molecular events, match them to the same sequence:
| Event | Sarcomere Change |
|---|---|
| Cross-bridge forms | I-band begins to narrow |
| Power stroke occurs | H-zone disappears |
| Full contraction | I-band minimum; A-band unchanged |
| Relaxation (Ca²⁺ pumped back) | Sarcomere returns to resting length |
NEET frequently asks which band does not change length during contraction. The answer is always the A-band — it spans the full length of the myosin filament, which physically doesn’t shorten.
When you see a diagram-based question showing band lengths, immediately identify the A-band as your fixed reference. Everything else narrows or disappears during contraction.
Common Mistake
Most students write that Ca²⁺ binds tropomyosin directly. This is wrong. Ca²⁺ binds troponin (specifically TnC). Tropomyosin is the physical blocker, but it’s troponin that acts as the calcium receptor and then mechanically shifts tropomyosin out of the way. In NEET 2024, this distinction was directly tested — roughly 40% of students marked the wrong molecule here.
A second trap: the question asks for “ATP hydrolysis” timing. The hydrolysis happens before the cross-bridge forms (to cock the myosin head), not after. Option B in our question gets this backwards — that’s exactly the distractor NEET uses.