Q.Which tissue is afflicted by Myasthenia gravis? What is the underlying cause?
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Mechanism Of Muscle Contraction
You are sitting still, reading this. Now clench your fist. In that instant, a signal shot from your brain down your arm, crossed a tiny gap onto a muscle fibre, and triggered a microscopic ratcheting motion inside thousands of cells. That ratcheting is muscle contraction.
The whole process is a chain of events that converts a chemical signal (nerve impulse) into a mechanical pull (shortening of the muscle). Let's walk through it step by step, from the nerve ending to the sliding filaments.
Step 1: The nerve impulse arrives and releases acetylcholine
A motor neuron carries an electrical signal to the neuromuscular junction — the point where the nerve meets the muscle fibre. When the impulse reaches the nerve terminal, it triggers the release of a chemical messenger called acetylcholine into the tiny gap (synaptic cleft).
Acetylcholine diffuses across and binds to receptors on the muscle cell membrane. This binding opens ion channels, causing a local electrical change that spreads across the muscle fibre's surface and deep into its interior via tube-like invaginations called T-tubules.
Acetylcholine is quickly broken down by an enzyme (acetylcholinesterase) so the signal is brief. This prevents the muscle from staying contracted.
Step 2: The T-tubule signal releases calcium from the sarcoplasmic reticulum
The electrical signal travelling down the T-tubules reaches the sarcoplasmic reticulum (SR) — a specialised calcium store wrapped around each contractile unit. The signal causes calcium channels on the SR to open, and calcium ions (Ca²⁺) flood into the cytoplasm surrounding the myofibrils.
This rise in calcium concentration is the master switch for contraction. Without calcium, the muscle stays relaxed.
Step 3: Calcium exposes the binding sites on actin
Inside each muscle fibre are two key protein filaments: actin (thin) and myosin (thick). In a relaxed muscle, a protein complex called troponin-tropomyosin sits on the actin filament, physically blocking the sites where myosin would attach.
Calcium binds to troponin, which changes shape and shifts the tropomyosin strand away, uncovering the myosin-binding sites on actin. Now the stage is set for the actual pulling.
Step 4: Cross-bridge cycling — the power stroke
Myosin heads are already "cocked" (energised) from a previous ATP hydrolysis. Each myosin head now binds to an exposed site on actin, forming a cross-bridge.
The myosin head then pivots, pulling the actin filament toward the centre of the sarcomere. This is the power stroke — the actual shortening of the muscle. After the power stroke, the myosin head is still attached to actin but in a low-energy position.
Think of a rowboat oar: the oar blade (myosin head) catches the water (actin) and pulls — that's the power stroke. Then you lift the oar out, reposition it, and pull again.
Step 5: ATP detaches the myosin and re-cocks it
For the cycle to repeat, the myosin head must let go of actin. A new molecule of ATP binds to the myosin head. This binding causes the myosin to release actin.
The ATP is then hydrolysed (split) into ADP and inorganic phosphate (Pᵢ), and the energy released re-cocks the myosin head back to its high-energy position. The head is now ready to bind to a new actin site further along the filament.
As long as calcium remains high and ATP is available, this cycle repeats hundreds of times per second, sliding the filaments past each other and shortening the muscle.
The cross-bridge cycle in four steps:
- Myosin head (cocked) binds to exposed actin → cross-bridge formed.
- Power stroke: myosin pivots, pulls actin → sarcomere shortens.
- ATP binds to myosin → myosin releases actin.
- ATP hydrolysed → myosin re-cocks.
Step 6: Relaxation — calcium is pumped back
When the nerve signal stops, calcium channels on the SR close. An active calcium pump (using ATP) pumps Ca²⁺ back into the SR, lowering the cytoplasmic calcium level.
Without calcium, troponin returns to its original shape, tropomyosin slides back over the binding sites, and myosin can no longer attach. The muscle relaxes.
The big picture: what drives it all …
Myasthenia gravis affects skeletal (voluntary) muscle, specifically at the neuromuscular junction, the point where a motor neuron hands its signal over to the muscle fibre. The underlying cause is an auto-immune reaction, in which the body's own immune system mistakenly attacks this junction. Because the nerve-to-muscle signal can no longer be properly transmitted, the affected muscles tire quickly, weaken, an …
Myasthenia gravis is an auto-immune disease that attacks the neuromuscular junction of skeletal muscle, causing rapid fatigue and weakness.
The tissue affected by myasthenia gravis is skeletal (voluntary) muscle, and more precisely the neuromuscular junction - the site where a motor neuron delivers its signal to the muscle fibre's plasma membrane (sarcolemma), also called the motor-end plate. Normal contraction depends on this junction releasing acetylcholine to trigger an action potential in the muscle fibre.
The underlying cause is auto-immune: the body's own defence system, which is meant to protect the body, instead mistakenly targets and attacks this very junction. With the nerve-to-muscle handover disrupted, the signal cannot be reliably passed on. …
- AP EAPCET 2026Set ap-2026-05-19-AN1 markMCQQ.Study the following statements regarding muscle contraction. I. During muscle contraction myosin heads attach to thin filaments forming cross-bridges. II. Calcium ions released from the sarcoplasmic reticulum bind to tropomyosin to expose active sites on thin filaments. III. Muscle fatigue occurs due to the accumulation of hydrochloric acid. IV. ATP is required for both the power stroke and the detachment of myosin heads from thin filaments. Identify the correct statements (A) I, III and IV (B) I and II (C) II and IV (D) I and IV
›Reveal solutionSolution
Cross-bridge formation (I) and ATP's dual role in the power stroke and head detachment (IV) are correctly stated; but Ca²⁺ binds troponin (not tropomyosin, II is wrong) and fatigue is from lactic acid (not HCl, III is wrong).
Concept and Intuition
The sliding filament theory explains muscle contraction through a repeating cross-bridge cycle. Calcium released from the sarcoplasmic reticulum binds specifically to troponin C (a subunit of the troponin complex sitting along the thin filament), which then causes tropomyosin — the actual filament that physically blocks the myosin-binding sites on actin at rest — to shift position and expose those sites. Statement II conflates troponin (the calcium sensor) with tropomyosin (the blocking protein it moves), making it inaccurate as worded. Once sites are exposed, myosin heads (energised by prior ATP hydrolysis) bind actin, forming cross-bridges (Statement I), and undergo a power stroke that pulls the thin filament inward. Crucially, ATP is needed twice in this cycle: first its hydrolysis (to ADP + Pi while still bound to the myosin head) powers the stroke, and second, fresh ATP binding to the myosin head (after the stroke) is what allows the head to detach from actin, ready for the next cycle — without ATP, myosin heads remain locked to actin, which is exactly the basis of rigor mortis (Statement IV, correct). Muscle fatigue during sustained exercise arises from a build-up of lactic acid from anaerobic glycolysis (not hydrochloric acid, an unrelated strong acid never produced by muscle metabolism), making Statement III false.
Step-by-Step Solution …
- AP EAPCET 2026Set ap-2026-05-20-AN1 markMCQQ.Study the following statements regarding muscle and identify incorrect statements. A) In mammals the sarcolemma penetrate between A and I bands to form T-tubule. B) Tetanus is caused due to accumulation of uric acid crystals. C) Troponin is distributed at regular intervals on tropomyosin. D) White muscle fibres have more mitochondria and depends on anaerobiosis. (A) A & C (B) B & C (C) B & D (D) A & D
›Reveal solutionSolution
This question tests fine details of skeletal muscle ultrastructure and physiology, requiring identification of the two false statements among four.
Concept and Intuition
Skeletal muscle fibres have a T-tubule system formed by inward extensions of the sarcolemma at the junction of the A and I bands, which helps synchronise excitation across the fibre. Regulatory proteins troponin and tropomyosin lie along the thin (actin) filament, with troponin molecules spaced at regular intervals on tropomyosin, controlling the exposure of myosin-binding sites. Physiological tetanus is a state of sustained contraction from rapidly repeated stimuli fusing individual twitches — it is unrelated to uric acid crystal deposition (which instead characterises gout). Fibre types differ in mitochondrial content and metabolism: red (slow, aerobic) fibres are rich in mitochondria and myoglobin, whereas white (fast, glycolytic) fibres have comparatively fewer mitochondria and rely predominantly on anaerobic glycolysis for ATP.
Step-by-Step Solution
- Evaluate A: sarcolemma forming T-tubules at the A-I junction is standard, correct muscle histology → TRUE.
- Evaluate B: tetanus (sustained contraction) is a stimulation-frequency phenomenon, NOT caused by uric acid crystal accumulation (that is gout) → FALSE.
- Evaluate C: troponin sitting at regular intervals along tropomyosin is a standard, correct description of thin-filament regulatory proteins → TRUE. …
- AP EAPCET 2022Set ap-2022-07-11-AN1 markMCQQ.Repeated activation of skeletal muscle leads to (A) Accumulation of lactic acid (B) Release of calcium ions (C) Glucose synthesis (D) Recovery from fatigue
›Reveal solutionSolution
Repeated stimulation of skeletal muscle outpaces oxygen supply, shifting metabolism to anaerobic glycolysis and causing lactic acid to accumulate, which is the classic cause of muscle fatigue.
Concept and Intuition
Skeletal muscle contraction requires a continuous ATP supply. Under normal, moderate activity, aerobic respiration (using oxygen delivered via blood) meets this demand. But with repeated/rapid activation, oxygen delivery cannot keep up, so the muscle switches partly to anaerobic glycolysis, converting pyruvate to lactic acid (lactate) instead of channelling it into the Krebs cycle. This lactic acid buildup lowers the local pH and interferes with muscle contraction machinery, producing the sensation and physiological state of fatigue.
Step-by-Step Solution
- Repeated activation increases the muscle's ATP demand rapidly.
- Oxygen supply via blood cannot increase fast enough to sustain fully aerobic respiration.
- The muscle shifts to anaerobic glycolysis as a supplementary ATP source.
- This produces lactic acid as an end product (instead of complete oxidation to CO2 and water). …
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