Locomotion and Movement — the Sliding Filament Theory, the Skeleton and Joints
The centrepiece is the sliding filament theory — the mechanism of muscle contraction — and it repays understanding one counter-intuitive fact: when a muscle shortens, the filaments themselves do not shorten; they slide past each other. Get that and the changes in the sarcomere bands fall into place. Around it sit two recall blocks: the structure of the muscle fibre (with the roles of calcium, troponin and ATP) and the skeleton and joints (the 206 bones grouped into axial and appendicular, and the joint types). The examiner's favourite trap is asking which bands change length during contraction — a question you can only answer if you have understood, not memorised, the sliding mechanism.
The Sliding Filament Theory
🎯 The filaments slide; they do not shrink
Contraction begins when a nerve impulse reaches the muscle and triggers the release of calcium ions from the sarcoplasmic reticulum. Calcium binds troponin, which shifts tropomyosin aside and uncovers the binding sites on actin. Now the myosin heads — energised by ATP — attach to actin, forming cross-bridges, and swivel, dragging the thin filaments toward the centre of the sarcomere. The head then binds a fresh ATP, detaches, re-cocks and repeats, walking the actin inward step by step. The crucial point is what does and does not change length. The actin and myosin filaments keep their own length throughout — nothing shrinks — but because the thin filaments are pulled deeper over the thick ones, the sarcomere shortens, the I band narrows, and the H zone narrows or disappears, while the A band stays exactly the same width (it is set by the myosin, which is not moving). A question asking "which band is unchanged during contraction" is testing precisely this: the A band. When the impulse stops, calcium is pumped back, the sites are re-covered, and the muscle relaxes.⚠️ No ATP does not mean a limp muscle — it means a stuck one
It is tempting to think ATP is only needed to make the muscle contract, so without it the muscle simply goes slack. The opposite is closer to the truth. ATP is needed for the myosin head to detach from actin after a stroke; without fresh ATP the cross-bridges cannot release, and the muscle stays locked — which is the biochemical basis of rigor mortis, the stiffening after death once ATP production ceases. ATP also powers the calcium pump that ends contraction, so relaxation is itself an energy-requiring, active process, not a passive collapse. The examinable takeaways are two: calcium starts contraction by exposing the binding sites, and ATP is spent both to power the power stroke and to detach the head for the next cycle.The Skeleton and Joints
- The adult human skeleton has 206 bones, in two divisions. The axial skeleton (80) — skull, vertebral column, ribs and sternum — forms the central axis. The appendicular skeleton (126) — limb bones plus the pectoral and pelvic girdles — hangs off it.
- The vertebral column has 26 vertebrae (cervical 7, thoracic 12, lumbar 5, plus the fused sacrum and coccyx); the rib cage has 12 pairs, the first seven "true", the next three "false", the last two "floating".
- Joints classify by mobility: fibrous (immovable, e.g. skull sutures), cartilaginous (slightly movable, e.g. between vertebrae) and synovial (freely movable — ball-and-socket at the shoulder/hip, hinge at the knee/elbow, pivot at the atlas–axis).
ℹ️ Common muscle and bone disorders worth naming
A short list of disorders reliably shows up. Myasthenia gravis is an autoimmune disease attacking the neuromuscular junction, causing fatigue and weakness of the skeletal muscles. Muscular dystrophy is progressive degeneration of muscle, largely genetic. Tetany is rapid, painful muscle spasms caused by a fall in blood calcium — tying neatly back to calcium's role in contraction. Arthritis is joint inflammation; osteoporosis is a loss of bone mass with age, linked to falling oestrogen after menopause, raising fracture risk; and gout is inflammation of joints from a build-up of uric acid crystals. Notice how two of these — tetany and gout — connect this chapter to earlier ones (calcium regulation and uric acid excretion), which is exactly the kind of cross-link NEET likes to test.Key takeaways
- Three muscle types: skeletal (striated, voluntary), smooth (unstriated, involuntary), cardiac (striated, involuntary).
- The sarcomere (between two Z lines) is the contractile unit; thick filament = myosin, thin filament = actin.
- During contraction filaments SLIDE, not shrink: sarcomere, I band and H zone narrow; the A band stays unchanged.
- Calcium uncovers actin binding sites (via troponin/tropomyosin) to START contraction.
- ATP powers the power stroke AND detaches the myosin head; no ATP → cross-bridges lock → rigor mortis.
- Skeleton: 206 bones = axial (80: skull, vertebral column, ribs, sternum) + appendicular (126: limbs, girdles).
- Joints: fibrous (immovable), cartilaginous (slightly movable), synovial (freely movable — ball-socket, hinge, pivot).
- Disorders: tetany (low blood Ca²⁺), gout (uric acid crystals), osteoporosis (low bone mass), myasthenia gravis (autoimmune NMJ).
Practice questions (8)
Attempt each one before opening the answer. Every explanation names the tempting wrong option as well as the right one, because that is where marks are lost.
During muscle contraction, which of the following remains unchanged in length?
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Answer: A — The A band
The A band equals the length of the myosin filament, which does not move, so it stays the same width throughout contraction. The I band and H zone narrow and the whole sarcomere shortens because the thin filaments slide inward, so those three all change.The immediate trigger that exposes the myosin-binding sites on actin is:
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Answer: A — Binding of calcium ions to troponin
Calcium released after a nerve impulse binds troponin, which moves tropomyosin off the binding sites so myosin can attach. A drop in calcium ends contraction rather than starting it, and ATP is hydrolysed by myosin, not actin, so the other options misassign the roles.Rigor mortis, the stiffening of muscles after death, occurs because:
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Answer: A — Without ATP the myosin heads cannot detach from actin
ATP is needed to release the cross-bridges; once ATP production stops after death, the myosin heads stay bound to actin and the muscle locks stiff. The effect comes from a lack of ATP, not from continued calcium release or water swelling, which is why the first option is correct.The adult human skeleton has 206 bones. The axial skeleton contributes:
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Answer: A — 80 bones
The axial skeleton — skull, vertebral column, ribs and sternum — has 80 bones, and the appendicular skeleton (limbs and girdles) has the remaining 126, together making 206. The 126 figure belongs to the appendicular division, offered here as the obvious distractor.A ball-and-socket joint, allowing movement in many directions, is found at the:
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Answer: A — Shoulder
The shoulder (and hip) is a ball-and-socket joint permitting movement in multiple planes. The knee and elbow are hinge joints allowing movement in essentially one plane, and skull sutures are fibrous, immovable joints, so none of those offers multidirectional movement.Tetany, marked by rapid painful muscle spasms, is caused by a fall in blood:
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Answer: A — Calcium
Low blood calcium disturbs the calcium signalling that controls contraction, producing the sustained spasms of tetany — a direct echo of calcium's trigger role in the sliding filament mechanism. Sodium, glucose and potassium imbalances cause other problems, not classical tetany.Which muscle type is striated but under involuntary control?
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Answer: A — Cardiac muscle
Cardiac muscle is striated like skeletal muscle but works involuntarily, beating without conscious control. Skeletal muscle is striated but voluntary, and smooth muscle is involuntary but unstriated, so cardiac uniquely combines striations with involuntary action.Osteoporosis, a decrease in bone mass raising fracture risk, is commonly linked in ageing women to a fall in:
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Answer: A — Oestrogen levels after menopause
Falling oestrogen after menopause reduces bone maintenance, lowering bone mass and raising fracture risk — the classic account of osteoporosis. Blood glucose, melanin and haemoglobin concern quite different systems and are not the recognised cause here.