Organismal Biology · Unit 5: Defense, movement and reproduction

Muscle, Bone and Movement

How does a nerve impulse become a pull on a bone, and why do skeletal, cardiac and smooth muscle, a tuna's red and white muscle, and a blowfly's flight muscle each do it differently? This lesson follows contraction from motor neuron to calcium to cross-bridge, compares the three muscle types and the fibre types, retells Pringle's recordings from insect flight muscle, and compares hydrostatic skeletons, exoskeletons and bone. Afterwards you can work out the force a muscle develops on a lever and say what a calcium-free bath tells you about how a muscle is triggered.

Watch first Filaments Slide, Nothing Shortens · 2:54

Hold a 2 kg bag in your hand with your elbow bent at a right angle, and in a simple lever model your biceps pulls with about seven and a half times that weight. Muscles are strong, but they are attached close to the joints they move. This lesson follows a contraction from the nerve to the protein that does the pulling, compares the muscles of hearts, guts, tuna and flies, and then looks at what muscles pull on.

From nerve to calcium to cross-bridge

A skeletal muscle fibre is one long cell with many nuclei, formed when embryonic muscle cells (myoblasts) fuse. It is packed with myofibrils, chains of repeating units called sarcomeres. Each sarcomere holds two kinds of filament: thick filaments of the protein myosin and thin filaments of actin. Their regular overlap makes the stripes you see under a microscope, which is why skeletal muscle is called striated.

The signal starts at the neuromuscular junction, the synapse between a motor neuron and a muscle fibre. The neuron releases acetylcholine, which opens channels in the fibre’s membrane and depolarizes it (synaptic transmission and the neuromuscular junction cover the details). That starts an action potential, an electrical signal that travels along the membrane (action potential). The signal runs down T tubules, infoldings of the membrane that reach deep into the fibre.

Next to each T tubule lies the sarcoplasmic reticulum (SR), the fibre’s internal calcium store. In vertebrate skeletal muscle, a voltage sensor in the T-tubule membrane (a channel called CaV1.1) is linked to the SR’s calcium release channel (RyR1). When the voltage changes, the sensor opens the release channel, and calcium floods out. Calcium entering from outside the cell is not required for this step.

Calcium binds troponin, a protein on the thin filament. Troponin then shifts tropomyosin, a strand that lies along actin and covers the sites where myosin binds. With the sites uncovered, myosin heads attach to actin, swing, and pull the thin filaments toward the middle of the sarcomere. These attached heads are cross-bridges.

This is the sliding filament model: the filaments do not get shorter; they slide past each other. The A band, which is the length of the thick filaments, keeps its width while the sarcomere shortens. Think of two combs pushed together tooth into tooth. The comb is the same length; the overlap changes.

ATP has two jobs here. First, at the myosin head: ATP binding releases the head from actin, and splitting the ATP re-cocks it for the next stroke. Second, pumps in the SR use ATP to move calcium back into the store, and as calcium falls, tropomyosin covers the sites again and the muscle relaxes. Without ATP, the heads stay stuck to actin, which is why muscles stiffen after death. How the cross-bridge cycle and the 1954 sliding filament papers fit together is told in molecular motors; troponin and calcium as a signal are in calcium signaling.

Three muscles, three triggers

Vertebrates have three kinds of muscle, built from the same actin and myosin but switched on differently.

AI-generated illustration: three panels comparing vertebrate muscle; long separate striped skeletal fibres, short branched striped cardiac cells joined end to end by gap junctions, and unstriped spindle-shaped smooth muscle cells with a gap junction between two neighbours.
Skeletal fibres are long, striped and unconnected; cardiac cells are short, branched, striped and joined by gap junctions; smooth muscle cells are unstriped, with gap junctions coupling neighbours in many smooth muscles, such as the gut wall. Skeletal and cardiac muscle use a troponin switch, smooth muscle calcium-calmodulin.

Skeletal muscle is striated and voluntary. Each fibre contracts when its own motor neuron fires, and fibres are not electrically connected to each other. Graded force comes from how many motor units fire and how often (motor units and reflexes).

Cardiac muscle is also striated, but its cells are short, branched and joined end to end by gap junctions, channels that let electrical current pass from cell to cell, so a wave of excitation spreads through the heart. No motor neuron starts the beat: pacemaker cells generate action potentials on their own, and nerves adjust their rate and the force of each beat (see circulation and the heart). The calcium trigger differs too. In heart cells, calcium entering through membrane channels during the action potential triggers a much larger release from the SR. The Fabiatos showed this calcium-triggered release in skinned cells from adult rat ventricles in 1975.

Smooth muscle lines the gut, blood vessels, airways and ducts. Its actin and myosin are not organized into sarcomeres, so it has no stripes. It is not under voluntary control; autonomic nerves, hormones and stretch act on it. In many smooth muscles, such as those of the gut wall, gap junctions couple neighbouring cells. Smooth muscle has no troponin switch. Instead calcium binds calmodulin, and calcium-calmodulin activates myosin light-chain kinase, an enzyme that adds a phosphate to the myosin light chain and turns myosin on. Chacko, Conti and Adelstein found in purified guinea-pig smooth muscle myosin that this phosphorylation raised its actin-activated ATPase activity.

Fast and slow: fibres, tuna and chickens

Skeletal fibres differ in speed and in how they make ATP. Slow oxidative fibres contract slowly, make most of their ATP by aerobic respiration, are rich in mitochondria and in myoglobin (an oxygen-binding protein, see oxygen transport), look dark red, and resist fatigue. Fast oxidative fibres contract quickly but still rely mainly on aerobic respiration. Fast glycolytic fibres contract quickly, rely on glycolysis (glycolysis), look pale, and fatigue sooner.

The names you read depend on the species. In humans the three main types are I, IIa and IIx. Human fibres long labelled IIb by staining turned out, in the 1994 study by Smerdu and colleagues, to express mostly IIx myosin, not the rodent IIb isoform.

Animals show the same split at the scale of whole muscles. In many fishes a thin band of dark red muscle runs along each side of the body under the skin and powers steady swimming, while the bulk of white muscle is used in bursts. In tunas the red muscle lies deeper, close to the backbone, and stays warmer than the water (thermoregulation). In domestic chickens, the leg muscles used in standing and walking are darker, and the breast muscles that power brief bursts of flapping are pale. Which fibres a muscle holds matches how it is used, not which animal it belongs to.

A fly’s wings outrun its nerves

In a locust or a dragonfly, each contraction of a flight muscle follows its own nerve impulse. That is synchronous muscle, the same rule as vertebrate skeletal muscle. Flies beat their wings much faster. In 1949 J. W. S. Pringle recorded from the flight muscles of tethered blue-bottle flies (Calliphora) in flight. If each contraction needed its own impulse, he expected one muscle action potential per wingbeat. He found far fewer impulses than wingbeats, and they were not timed to particular beats.

AI-generated illustration: a blue-bottle fly held by a rod on its back, wings blurred in motion, with a fine electrode in its thorax connected by a wire to a plain recording box; an inset shows a springy thorax box pressed by two flight muscles with a nerve keeping them switched on.
Pringle recorded from the flight muscles of tethered blue-bottle flies (Calliphora) as they beat their wings. He found far fewer impulses than wingbeats, so he concluded that the muscle and the springy thorax set the beat while nerve impulses keep the muscle switched on.

His conclusion: in these flies the beat is set by the muscle and the springy thorax it pulls on, and nerve impulses keep the muscle switched on. This is asynchronous muscle, found in flies, bees and wasps, beetles and some other insects. Asynchronous does not mean nerveless; without impulses the muscle stops. The recordings did not show how the muscle oscillates. Later work on isolated beetle flight muscle by Machin and Pringle (1959) reported that the muscle is activated by being stretched: as one muscle pulls, it stretches its antagonist, which then contracts.

Skeletons: water, armour and bone, with levers

Muscles only pull, so every muscle works against something that stretches it back. A hydrostatic skeleton is fluid under pressure in a closed cavity. An earthworm contracts the muscles of its body wall against fluid in its body cavity, so each segment can lengthen or shorten (animal body plans). A muscular hydrostat has no fluid cavity: octopus arms and mammalian tongues are mostly muscle at constant volume, so muscle in one direction acts against muscle in another.

AI-generated illustration: three panels comparing skeletons; a cut-open earthworm segment with fluid in its body cavity, an octopus arm with solid muscle and no cavity, and a crab leg whose hard outer case holds muscle attached inside.
Muscles only pull, so each needs something to pull against: fluid under pressure in an earthworm's body cavity, other muscle at constant volume in an octopus arm or a mammalian tongue, or a hard outer case, as in crabs and insects.

An exoskeleton is a hard outer case with muscles attached inside, as in insects and crabs. It cannot grow, so arthropods shed it and make a larger one at each moult (endocrine system). An endoskeleton lies inside the soft tissues, as in vertebrates.

Bone is living tissue. Its matrix combines collagen fibres with a calcium phosphate mineral, hydroxyapatite. Compact bone forms the dense outer wall and is built of osteons, cylinders of matrix around a central canal. Spongy bone, inside, is a lattice of thin struts called trabeculae. Osteoblasts lay down new bone, osteoclasts dissolve it, and osteocytes are former osteoblasts trapped in the matrix. Because bone is resorbed and rebuilt throughout life, its shape changes with the loads it carries (on how bone thickness scales with body size, see size and scaling).

Bones meet at joints. In humans, joints are grouped by structure as fibrous (bones joined by connective tissue, as in skull sutures), cartilaginous (joined by cartilage) or synovial (a lubricated, fluid-filled cavity, as at the elbow and knee). At a synovial joint muscles work as antagonistic pairs: the biceps bends the elbow and the triceps straightens it. Tendons carry the pull to bone, and the bone acts as a lever.

Worked problem. These numbers are invented for an idealized model. A forearm is held horizontal and treated as weightless. A 20 N load (about 2 kg) is held in the hand 0.30 m from the elbow. The biceps pulls straight up with a moment arm of 0.040 m. Assume static equilibrium, with the elbow as the pivot.

muscle force x muscle moment arm = load x load arm

  1. Torque from the load. 20 N x 0.30 m = 6.0 N m.
  2. Muscle force. F x 0.040 m = 6.0 N m, so F = 6.0 / 0.040 = 150 N, which is 7.5 times the load.
  3. Check. 150 N x 0.040 m = 6.0 N m, matching the load’s torque.
  4. What the trade buys. The same geometry means the hand moves 0.30 / 0.040 = 7.5 times as far, and as fast, as the point where the biceps attaches. If the biceps shortens by 1.0 cm, the hand moves about 7.5 cm (for a small angle). This is a third-class lever: the muscle pulls between the pivot and the load, and gives up force for distance and speed.
Elbow lever: force traded for distance and speed⚙ original · interactive
View
Load torque
Muscle force
Muscle force as a multiple of the load
Hand movement per 1.0 cm of muscle shortening

In this sketch: invented numbers, an idealized weightless forearm held horizontal, static equilibrium, the biceps pulling straight up, the elbow as the pivot; not anatomy.

Rule to keep: muscle force x muscle moment arm = load x load arm. A short moment arm means a large muscle force, and the same ratio means the hand moves that many times as far and as fast as the muscle’s attachment (for a small angle).

Design problem

Does a muscle require calcium from outside the cell to contract? You have frog skeletal muscle fibres and isolated cardiac cells, a calcium-free bathing solution with a calcium binder, and a drug that blocks the L-type calcium channels in the cell membrane. Design an experiment that tells the two triggers apart.

One way to do it

Stimulate each preparation electrically and record force, first in normal solution and then after switching to the calcium-free solution, and in a separate run with the channel blocker added to normal solution.

The prediction for skeletal fibres: twitches continue for a time without calcium entry, because the voltage sensor is linked mechanically to the SR release channel. Force should fade only slowly, as the internal store runs down. For cardiac cells: force falls within a few beats in calcium-free solution and drops with the blocker, because entering calcium triggers SR release, as the Fabiatos’ skinned rat ventricular cells suggested.

Controls matter. Record action potentials in every condition, so that a loss of force cannot be blamed on a membrane that no longer fires. Return each preparation to normal solution to show that the effect reverses and the cells were not damaged. Use cells from the same animals and the same temperature. Name the species in your conclusion: the result is about frog skeletal muscle and the heart cells you used. The older story of Ringer’s frog heart and bath calcium is told in calcium signaling.

How we measure it

Electrical recording from working muscle

Place fine electrodes in or on a muscle and record its action potentials while the animal moves, here a tethered fly beating its wings. Counting impulses against movements tells you whether each contraction follows its own impulse.

Skinned muscle cells with calcium buffers

Remove the surface membrane from a muscle cell, mechanically or with detergent, so that the experimenter sets the calcium, ATP and other contents of the bath. The Fabiatos used this in rat ventricular cells to separate calcium acting on the filaments from calcium released by the sarcoplasmic reticulum.

Myosin typing by histochemistry and in situ hybridization

Stain muscle sections for myosin ATPase activity, which differs among fibre types, and probe neighbouring sections for the messenger RNA of each myosin heavy chain. Smerdu and colleagues used both on human muscle and found that fibres stained as IIb carry IIx myosin transcripts.

Protein purification and enzyme assays

Purify a protein from a tissue, change it (here by adding or removing phosphate), and measure its activity. Chacko, Conti and Adelstein used this on guinea-pig smooth muscle myosin.

Finish line

Test yourself

8 questions

Practice and MCAT-style, with explained answers.

Next · Lesson 20

Animal Reproduction

A monkey's pituitary could not sustain its output on a steady drip of the hypothalamic hormone, yet sustained it when the same hormone was given once an hour. Why does timing matter?

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J. W. S. Pringle

J. W. S. Pringle

Recorded muscle action potentials from the flight muscles of flies while timing their wingbeats (1949), and found far fewer impulses than wingbeats, evidence that in these insects the muscle and thorax set the beat while the nerve keeps the muscle active.

In vertebrate skeletal muscle, and in the flight muscle of locusts, each contraction follows its own nerve impulse. Flies beat their wings far faster than that rule seemed to allow, and John Pringle, a zoologist at Cambridge, asked whether the rule held for them. He held blue-bottle flies (Calliphora) tethered so that they would beat their wings in place, put a fine electrode into the flight muscle, and recorded the muscle's electrical activity during flight. If every contraction needed its own impulse, impulses and wingbeats should match one for one. They did not. The muscle fired far less often than the wings beat, and the impulses were not locked to particular beats. He concluded that in these flies the rhythm comes from the muscle and the elastic thorax it drives, and the nerve keeps the muscle switched on. Pringle had suggested in 1949 that the muscle is excited to respond to stretch. A decade later, Machin and Pringle studied isolated flight muscle from a beetle and reported that it is activated by being stretched. That work, with later studies, is how biologists now explain the high wingbeat rates of flies, bees and beetles.

✓ verbatim Pringle, The excitation and contraction of the flight muscles of insects, Journal of Physiology 108:226-232 (1949); Machin and Pringle, The physiology of insect fibrillar muscle II, Proceedings of the Royal Society B 151:204-225 (1959).
Alexandre Fabiato and Françoise Fabiato

Alexandre Fabiato and Françoise Fabiato

Showed in skinned cells from adult rat ventricles (1975) that a small rise in calcium can trigger a much larger release of calcium from the sarcoplasmic reticulum, the trigger that sets cardiac muscle apart from skeletal muscle.

A heart cell's outer membrane lets calcium in with each beat, and the cell also holds calcium in its internal store, the sarcoplasmic reticulum. Which one starts the contraction? The Fabiatos removed the outer membrane altogether. They took cell fragments from adult rat ventricles, stripped them mechanically of their surface membrane (a "skinned" cell), and measured each fragment's tension with a photodiode force transducer while they set the calcium in the bath. With strong calcium buffering, 4.0 mM of the calcium binder EGTA, tension simply followed the bath calcium, and destroying the sarcoplasmic reticulum with the detergent Brij 58 left that relation unchanged: here calcium was acting on the filaments directly. With weak buffering, 0.050 mM EGTA, the fragments contracted in repeated cycles. They concluded that calcium triggered the release of calcium from the sarcoplasmic reticulum. The work gave cardiac physiology its central idea of calcium-triggered calcium release, tested here in rat cells without an intact membrane.

✓ verbatim Fabiato and Fabiato, Contractions induced by a calcium-triggered release of calcium from the sarcoplasmic reticulum of single skinned cardiac cells, Journal of Physiology 249:469-495 (1975).
S. Chacko, M. A. Conti and R. S. Adelstein

S. Chacko, M. A. Conti and R. S. Adelstein

Purified smooth muscle myosin from guinea-pig vas deferens and reported (1977) that phosphorylating its 20,000-dalton light chain increased its actin-activated ATPase activity, and dephosphorylating it decreased that activity.

Skeletal muscle is switched on at the thin filament, where calcium moves troponin and tropomyosin aside. Smooth muscle, which lines the gut, blood vessels and ducts, has no troponin switch, so how does calcium turn it on? Chacko, Conti and Adelstein worked with the vas deferens of the guinea pig, the muscular duct that carries sperm. From it they prepared an actomyosin fraction that contained the enzymes for adding and removing phosphate groups, and purified the myosin. A small subunit of the myosin, a light chain of about 20,000 daltons, became phosphorylated. When it was, the myosin's actin-activated ATPase, its rate of splitting ATP in the presence of actin, rose markedly; when the phosphate was removed, the activity fell. The paper located a smooth muscle switch on the myosin itself rather than on actin. It made possible the textbook picture in which calcium, through calmodulin and a kinase, phosphorylates myosin to start contraction, a picture built from this purified guinea-pig preparation and later work.

✓ verbatim Chacko, Conti and Adelstein, Effect of phosphorylation of smooth muscle myosin on actin activation and Ca2+ regulation, Proceedings of the National Academy of Sciences USA 74:129-133 (1977).
Test yourself
Question 1 of 8 Score 0 / 0

In vertebrate skeletal muscle, which protein binds calcium and so allows tropomyosin to move off the myosin-binding sites on actin?
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Every structure, slide, simulation, and clip on this page is listed below with the source it came from. None of the 3D structures is drawn by hand or by AI: each one loads by accession ID from RCSB PDB or PubChem. This panel is generated from the lesson's own data file, so what it lists is what the page loads.

Simulations

  • The forearm as a lever · Original interactive — Biochemistrypedia (Deppmann Lab).

Scientist profiles & quotes

  • J. W. S. Pringle — Pringle, The excitation and contraction of the flight muscles of insects, Journal of Physiology 108:226-232 (1949); Machin and Pringle, The physiology of insect fibrillar muscle II, Proceedings of the Royal Society B 151:204-225 (1959).
  • Alexandre Fabiato and Françoise Fabiato — Fabiato and Fabiato, Contractions induced by a calcium-triggered release of calcium from the sarcoplasmic reticulum of single skinned cardiac cells, Journal of Physiology 249:469-495 (1975).
  • S. Chacko, M. A. Conti and R. S. Adelstein — Chacko, Conti and Adelstein, Effect of phosphorylation of smooth muscle myosin on actin activation and Ca2+ regulation, Proceedings of the National Academy of Sciences USA 74:129-133 (1977).

Quotes are verbatim from the cited source. Profile text is original to this site and was checked against the sources cited.

Animated explainer

Filaments Slide, Nothing Shortens · narration: an AI narrator voice (Gemini, Charon) reading narration written from this lesson's text · animation: AI-generated in code (Manim) by Claude, a schematic with no drawn molecular structures, plots computed from their equations · captions from the narration script.

Images & figures

3 illustrations in this lesson are AI-generated: drawn by an image model from a written spec, then checked by a separate AI judge against the spec and the lesson text. None shows a chemical structure or data.

  • three panels comparing vertebrate muscle; long separate striped skeletal fibres, short branched striped cardiac cells joined end to end by gap junctions, and unstriped spindle-shaped smooth muscle cells with a gap junction between two neighbours.
  • a blue-bottle fly held by a rod on its back, wings blurred in motion, with a fine electrode in its thorax connected by a wire to a plain recording box; an inset shows a springy thorax box pressed by two flight muscles with a nerve keeping them switched on.
  • three panels comparing skeletons; a cut-open earthworm segment with fluid in its body cavity, an octopus arm with solid muscle and no cavity, and a crab leg whose hard outer case holds muscle attached inside.

Every 3D structure is rendered live from an accession ID, and every plot is drawn from its equation in the browser.

integrity Machines check the mechanics. The build confirms that every local file exists, that every question's answer key points at a real choice, and that any AI-generated scientific figure names the person who checked it; a weekly job re-resolves every accession ID against its database. Questions are original; MCAT-style items are written for this site and are not real AAMC questions. Banned sources (the Tymoczko textbook, publisher decks, copyrighted figures) are not used.

Like I'm five

Your muscles are made of tiny ropes and tiny hands. When your brain sends a message, the hands grab the ropes and pull them closer together, and the muscle gets shorter. Muscles can only pull, so your arm has one muscle to bend it and another to straighten it. Your bones are the sticks they pull on.
High school

A nerve releases a chemical onto a muscle fibre, which starts an electrical signal. The signal makes the fibre release calcium from an internal store, and calcium uncovers spots on thin actin filaments where myosin heads can grab. The heads pull the thin filaments past thick ones, so the muscle shortens without any filament getting shorter. ATP lets each head let go and also powers the pumps that put calcium away so the muscle relaxes. Heart and gut muscle use the same proteins but are switched on differently. Muscles pull on skeletons, which can be water under pressure (earthworms), an outer case (insects) or bone (vertebrates).
College

Acetylcholine at the neuromuscular junction depolarizes a skeletal fibre; the action potential spreads along the sarcolemma and down T tubules, where a voltage sensor (CaV1.1) linked to the ryanodine receptor releases calcium from the sarcoplasmic reticulum without needing calcium entry. Calcium binds troponin, tropomyosin moves, and myosin cross-bridges cycle, with ATP binding releasing each head and ATP hydrolysis re-cocking it; SR pumps use ATP to restore resting calcium. Cardiac muscle relies on calcium entry to trigger SR release and is coupled by gap junctions; smooth muscle uses calcium-calmodulin and myosin light-chain kinase. Fibre types differ in myosin isoform and in oxidative or glycolytic capacity. Skeletal muscles act on bones as levers, usually with short moment arms that trade force for speed and distance.
Graduate

For a static joint, torque balance gives F_muscle = F_load x (load arm / muscle moment arm), and the same ratio sets how far and how fast the distal segment moves per unit muscle shortening (small-angle approximation). With a 0.040 m moment arm and a 0.30 m load arm, the ratio is 7.5. In asynchronous insect flight muscle the contraction frequency is set by the mechanical resonance of the muscle and thorax, not by the motor neuron firing rate, so wingbeat frequency can exceed impulse frequency several-fold or more. The open question is how stretch activation works at the molecular level: how stretching the filament lattice raises the force of an already calcium-activated fibre is still being worked out, with proposals involving troponin isoforms specific to these muscles and the geometry of thick and thin filaments.
Rigor mortis is a cross-bridge story

After death, a muscle cell eventually can no longer make enough ATP. The myosin heads that were attached to actin stay attached, because ATP binding is what releases them, so the muscles stiffen, the state called rigor mortis. The stiffness later passes as the muscle proteins break down. It is a visible demonstration that relaxing a muscle takes energy too: without ATP the heads cannot let go, and the pumps that put calcium back in its store stop working.

— Betts and colleagues, Anatomy and Physiology 2e, OpenStax (2022), section 10.3.
Human IIb fibres are not rodent IIb fibres

Fast human muscle fibres were long divided by an ATPase stain into IIa and IIb, borrowing names from rodent muscle, where IIb myosin is a distinct, very fast isoform. Smerdu and colleagues located the messenger RNA for each myosin heavy chain in human muscle sections by in situ hybridization. The fibres that stained as IIb preferentially expressed IIx myosin transcripts, and some fibres were hybrids expressing two neighbouring types. Human fast fibres are now usually called IIa and IIx, and a rodent result about IIb fibres cannot be read straight across to people.

— Smerdu, Karsch-Mizrachi, Campione, Leinwand and Schiaffino, American Journal of Physiology 267:C1723-C1728 (1994).
Tongues, tentacles and trunks

An earthworm moves by squeezing fluid in a body cavity. William Kier and Kathleen Smith pointed out that some organs do the same job with no cavity at all: the tongues of mammals and lizards, the arms and tentacles of squid and octopuses, and the elephant's trunk. They called these muscular hydrostats. Muscle tissue keeps a nearly constant volume, so if fibres running around an octopus arm contract and make it thinner, it must get longer. Muscle arranged in several directions lets such an organ bend, twist and stiffen.

— Kier and Smith, Tongues, tentacles and trunks: the biomechanics of movement in muscular-hydrostats, Zoological Journal of the Linnean Society 83:307-324 (1985).

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