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Week 10 · Chapter

Chapter 10 — Muscle Tissue & the Physiology of Contraction

Human Anatomy and Physiology I Free sample edition

The module's primary reading · ~40–50 minutes · Objective 5 (explain skeletal-muscle structure from the whole muscle to the sarcomere, the sliding-filament model, and the ordered steps of excitation, contraction, and relaxation at the neuromuscular junction and inside the fiber, and describe the organization of the muscular system — origin and insertion, muscle teams, lever classes, and the major muscles by region and action), Objective 2 (relate the chemistry of the body to its function — atoms and the three bond types, water's properties, the logarithmic pH scale with the blood's buffered range, and the four classes of organic compounds — and explain the cell's membrane, organelles, and transport (diffusion, osmosis and tonicity, active transport, and bulk transport), the overview of how a cell makes ATP, and how a gene is read into a protein) · Read it first this week; the lecture, the slides, the tutorial, the quiz, and the lab all build on it.

In plain language

Every move you make, from a blink to a sprint, starts when a muscle pulls. This week you look inside one skeletal muscle and follow a single command from a nerve to the tiny moving parts that do the pulling. You meet the sarcomere (the smallest unit in a muscle that can shorten) and the two kinds of strands inside it that slide past each other. You put the steps of a contraction in their fixed order, and you see why the fuel molecule ATP is needed to let go as well as to pull. You finish by reading a set of grip counts to see what fatigue (a muscle's falling ability to keep contracting) looks like in numbers.

Why you already care about this

Grab a tennis ball, or roll up a pair of socks. Squeeze it as many times as you can in 10 seconds. Rest for 15 seconds, then do it again, for 5 rounds in all. By the fourth or fifth round your hand slows down, and your forearm may ache or burn. Nothing in your hand broke, and the same muscle is still there. So what changed?

You have felt the same thing on a long hike up a hill, when your legs lose their snap near the top, or while carrying heavy grocery bags from the car, when your grip starts to slip. A pet that tugs hard on its leash for a whole walk can leave your fingers stiff and slow. Each of those moments is the same set of tiny pulls inside your muscle fibers getting harder to keep up.

By the end of this chapter you will be able to:

name the levels of a skeletal muscle from the whole muscle down to the sarcomere, with the wrapping at each level;
label a sarcomere's Z discs, thin filaments of actin, thick filaments of myosin, and the troponin and tropomyosin on the thin filament;
explain the sliding filament model and say why the A band keeps its width;
put the five steps of excitation-contraction coupling in order, with the place each step happens;
name ATP's three jobs in a muscle fiber and say why rigor mortis follows death;
run relaxation as an ordered, ATP-costing shutdown;
tell slow oxidative fibers from fast glycolytic fibers and define a motor unit;
add, average, and find the drop and the percent decline for a grip-fatigue series, and read the trend as fewer cross-bridges cycling.

Carry this line with you: the filaments slide; they do not shrink.

Where we are

Already covered: Week 2, The Chemistry of Life, gave you ATP, the energy molecule cells spend. Week 3, The Cell & Membrane Transport, gave you membranes, ions such as Ca²⁺, and pumps that move ions using ATP. Week 4, Cellular Energy & Protein Synthesis, showed that a cell short on oxygen makes lactic acid. Week 5, Tissues, introduced skeletal muscle as long, striated, multinucleate, voluntary tissue. Week 9, The Skeleton & Joints, gave you the joints that muscles move.
This week: the skeletal-muscle hierarchy, the sarcomere, the sliding filament model, the ordered steps of excitation-contraction coupling, ATP's three jobs, relaxation, motor units, fiber types, and fatigue read on the grip-fatigue series.
How they connect: the muscle fiber is a cell, so everything you learned about membranes, ions, pumps, and ATP happens inside it on a large scale.
Where we're going next: Week 11, The Muscular System, steps back out to whole muscles, how they team up, and how bones act as levers.

Here is what you lean on this week. In Week 5 you saw skeletal muscle under a microscope: long, cylindrical, striated fibers with many nuclei at the edge of each cell, under voluntary control. In Week 3 you learned that a membrane can hold ions on one side, and that a pump spends ATP to move ions against their gradient. In Week 4 you learned that when oxygen runs short, pyruvate becomes lactic acid. This week puts all of those into one working cell.

1. Climb down the hierarchy: from whole muscle to sarcomere

Think of a thick rope. Pull it apart and it is made of smaller cords. Each cord is made of strands, and each strand is made of fibers. Skeletal muscle is built the same way, one bundle inside another, so a pull made at the smallest level adds up to a pull on a bone.

Here is the ladder, from big to small:

the whole muscle, such as the muscle in your forearm that closes your hand;
a fascicle, a bundle of muscle fibers inside a whole muscle, wrapped by the perimysium;
a muscle fiber, one skeletal muscle cell, long and with many nuclei, whose membrane is the sarcolemma and whose cytoplasm is the sarcoplasm;
a myofibril, a strand inside a muscle fiber made of sarcomeres, the level between the fiber and the sarcomere;
a sarcomere, the functional unit of a myofibril, running from one Z disc to the next, where thin and thick filaments overlap and slide.

The fiber's membrane has its own name. The sarcolemma is the plasma membrane of a muscle fiber, along which the muscle action potential travels. The sarcoplasm is the cytoplasm of a muscle fiber.

Connective tissue wraps every level, the way a sleeve wraps each cord in a rope. The epimysium is the connective-tissue wrapping around a whole skeletal muscle. The perimysium is the connective-tissue wrapping around each fascicle inside a muscle. The endomysium is the connective-tissue wrapping around each muscle fiber.

Worked example — climb down and wrap. You start at a whole forearm muscle and climb down to the unit that shortens, naming the wrapping where there is one.

Whole muscle, wrapped by the epimysium.
Fascicle, wrapped by the perimysium.
Muscle fiber, one cell, wrapped by the endomysium.
Myofibril, a strand inside the fiber.
Sarcomere, the unit that shortens.
In one line: muscle → fascicle → muscle fiber → myofibril → sarcomere.

Misconception check. Students often think a muscle fiber is a thread made of many cells, like a fiber in a sweater. It is tempting because "fiber" sounds like yarn. The cure: in muscle, one fiber is one cell, a very long cell with many nuclei. The many-cell bundle is the fascicle. A memory aid for the wrappings: epi is upon the whole muscle, peri is around a fascicle, and endo is within, around each fiber.

2. Open a sarcomere: actin is thin, myosin is thick

Picture a short stretch of a myofibril under a strong microscope, with dark and light bands lined up across it. One sarcomere is the stretch between two boundary lines. Inside it, two kinds of protein strands lie side by side, overlapping like the fingers of two hands laced together.

A Z disc is the boundary at each end of a sarcomere, where the thin filaments anchor; the Z discs move closer together when the sarcomere shortens.
A thin filament is the filament anchored to the Z discs, made of actin and carrying the regulatory proteins troponin and tropomyosin.
Actin is the protein of the thin filament, with binding sites that myosin heads grab during contraction.
A thick filament is the filament in the middle of the sarcomere, made of myosin and carrying many heads.
Myosin is the protein of the thick filament, whose heads attach to actin and pull it during contraction.

Two more proteins ride along the thin filament and act like a safety cover. Tropomyosin is a regulatory protein along the thin filament that covers actin's binding sites while the fiber is at rest. Troponin is a regulatory protein on the thin filament that binds Ca²⁺ and then moves tropomyosin off actin's binding sites. While the cover is on, the myosin heads have nothing to grab.

Worked example — label a sarcomere from one end to the other. You read a described sarcomere from left to right.

Left boundary: a Z disc.
Anchored to it and reaching inward: thin filaments of actin, with troponin and tropomyosin along them.
In the middle: thick filaments of myosin, each with many heads pointing toward the thin filaments.
Reaching inward from the right: more thin filaments of actin.
Right boundary: the next Z disc.
In one line: Z disc → actin → myosin → actin → Z disc.

Misconception check. Students often call actin the thick filament. It is tempting because actin is the one that moves, and the moving part feels like it should be the big one. The cure: myosin is the thick filament, and it carries the heads. Say "thick myosin, with heads; thin actin, on the Z discs" until it sticks.

3. Wire the fiber: T-tubules and the sarcoplasmic reticulum

A muscle fiber is very long, and its sarcomeres sit deep inside it. A signal that stayed on the outer surface would reach the inner sarcomeres late. The fiber solves this with two parts that work as a pair, the way a building has both wiring that reaches every room and a supply closet on every floor.

T-tubules are passages that carry the muscle action potential from the sarcolemma deep into the muscle fiber.
The sarcoplasmic reticulum is the membrane store inside a muscle fiber that holds Ca²⁺, releases it to start contraction, and takes it back with ATP-powered pumps.

You met this kind of membrane store in Week 3, when the smooth ER regulated Ca²⁺. In a muscle fiber the store is specialized for one job: hold the calcium until the signal arrives, then let it go.

Worked example — say what each part carries. You sort two things that move inside a fiber.

The electrical signal moves along the sarcolemma and then inward through the T-tubules.
Ca²⁺ is held in the sarcoplasmic reticulum, released when the signal arrives, and pumped back afterward.
In one line: the T-tubules carry the signal; the sarcoplasmic reticulum holds and releases the calcium.

Misconception check. Students often think the T-tubules store the calcium, because both parts sit side by side inside the fiber. The cure is to give each part one verb. The T-tubules carry the signal. The sarcoplasmic reticulum stores, releases, and takes back Ca²⁺.

4. Slide, do not shrink: the sliding filament model

Lace the teeth of two combs together a little way. Now push the combs toward each other. The pair gets shorter, yet not one tooth got shorter. The teeth slid into more overlap. That is the whole idea of this section.

The sliding filament model is the classroom model of contraction in which thin filaments are pulled past thick filaments, so the sarcomere shortens while neither filament gets shorter. When the fiber contracts, the thin filaments are pulled toward the center of the sarcomere. The Z discs move closer. The sarcomere shortens.

One band gives the model away. The A band is the band of a sarcomere where the thick filaments lie; it keeps its width during contraction because the filaments do not shorten. If the filaments themselves shrank, the A band would shrink too. It does not.

The model has a history you can place. It was proposed in two papers published side by side in the journal Nature in 1954: one by A. F. Huxley and R. Niedergerke, and one by H. E. Huxley and J. Hanson. These are two different scientists named Huxley. The sliding filament model is a model: a simplified picture you can hold in one hand, not a description of every detail in every fiber.

Worked example — predict what changes in a contraction. You list four parts of a sarcomere and say whether each gets shorter, moves, or stays the same.

The sarcomere as a whole: shortens, because the Z discs move closer.
The Z discs: move toward each other.
The thin filaments of actin: slide toward the center but keep their length.
The thick filaments of myosin, and so the A band: keep their length and width.

Misconception check. Students often say "the filaments shorten when a muscle contracts." It is tempting because the muscle gets shorter, so it seems every part inside must too. The cure is the A band. It keeps its width, so the thick filaments did not shrink, and the thin filaments slid. Carry the line: the filaments slide; they do not shrink.

5. Put contraction in order: excitation-contraction coupling

Think of a row of dominoes. Each one falls only after the one before it. A contraction works the same way, and in this course the order is a fact you are graded on. Each step also has a place, so you say the order and name the place.

Excitation-contraction coupling is the ordered chain of events that links a motor neuron's signal to the pull of the myosin heads: ACh release, the muscle action potential, Ca²⁺ release, Ca²⁺ binding troponin, and the power stroke.

Five terms come with the chain:

A motor neuron is a nerve cell that carries a command to skeletal muscle fibers and releases acetylcholine at the neuromuscular junction.
The neuromuscular junction is the meeting point between a motor neuron's ending and a muscle fiber, where acetylcholine crosses the synaptic cleft to the motor end-plate.
Acetylcholine is the chemical messenger, written ACh, that a motor neuron releases at the neuromuscular junction to trigger the muscle fiber's own electrical signal.
The synaptic cleft is the narrow gap between a nerve ending and the cell it signals, which a chemical messenger crosses.
The motor end-plate is the region of the sarcolemma at the neuromuscular junction that receives acetylcholine.

Here are the five steps:

At the junction. The motor neuron's signal reaches the neuromuscular junction and releases ACh across the synaptic cleft to the motor end-plate.
Along the sarcolemma and down the T-tubules. ACh triggers the muscle's own electrical signal. The muscle action potential is the muscle fiber's own electrical signal, triggered by acetylcholine and carried along the sarcolemma and down the T-tubules. How that electrical signal works in detail waits for Week 12; for now, the muscle fires its own electrical signal.
At the sarcoplasmic reticulum. The sarcoplasmic reticulum releases Ca²⁺.
On the thin filament. Ca²⁺ binds troponin, which moves tropomyosin off actin's binding sites. The cover comes off.
Between the filaments. Myosin heads attach to actin. A cross-bridge is the link formed when a myosin head attaches to a binding site on actin. The power stroke is the pull of an attached myosin head that drags the thin filament toward the center of the sarcomere, using ATP.

Worked example — fix a scrambled chain. A study card lists the steps as: Ca²⁺ released; ACh at the junction; power stroke; Ca²⁺ binds troponin; muscle action potential. You put them in order and write the chain.

Find the trigger: ACh at the neuromuscular junction comes first, because nothing happens in the fiber until the nerve signals.
Next, the fiber's own signal: the muscle action potential along the sarcolemma and down the T-tubules.
Then the store opens: Ca²⁺ released from the sarcoplasmic reticulum.
Then the cover moves: Ca²⁺ binds troponin, and tropomyosin uncovers actin.
Last, the pull: cross-bridge and power stroke.
In one line: ACh at the neuromuscular junction → muscle action potential down the T-tubules → Ca²⁺ from the sarcoplasmic reticulum → Ca²⁺ binds troponin and tropomyosin uncovers actin → cross-bridge and power stroke (ATP).

Misconception check. Two slips travel together here. First, students often put calcium before the nerve signal, because calcium feels like the "on switch." ACh comes first; calcium is step 3. Second, students often say the neuromuscular junction releases calcium. The junction releases ACh. The calcium comes from the sarcoplasmic reticulum, inside the fiber.

6. Follow the fuel: ATP's three jobs

Think of a climber on a rock wall. To move up, the climber has to grab a hold, pull, and then let go so the hand can reach the next hold. Letting go takes effort too. A myosin head works the same way, and ATP pays for more than the pull.

ATP has three jobs in a working muscle fiber:

The pull. ATP powers the power stroke.
The release. A fresh ATP binding to a myosin head releases the head from actin, so the head can grab again.
The cleanup. ATP runs the pumps that move Ca²⁺ back into the sarcoplasmic reticulum.

Job 2 explains a well-known fact about death. Rigor mortis is the stiffness that follows death, because without ATP the myosin heads cannot release from actin. The heads stay locked to actin, so the muscles stay stiff.

Worked example — what stops without ATP? You take ATP away and check each job.

The pull: no new power strokes.
The release: heads already attached cannot let go, so they stay locked, which is rigor mortis.
The cleanup: Ca²⁺ cannot be pumped back into the sarcoplasmic reticulum.
In one line: no ATP, no pull, no release, no cleanup.

Misconception check. Students often think ATP is needed only to contract. It is tempting because "energy for movement" sounds like energy for pulling. The cure is rigor mortis: without ATP, a muscle does not go limp; it locks. ATP pays for the power stroke, for releasing the head, and for the calcium pumps.

7. Run relaxation in order: an active shutdown

Relaxing feels like doing nothing. Let your hand fall open after a squeeze and it seems effortless. Inside each fiber, though, relaxation is its own ordered set of steps, and one of them costs ATP.

Relaxation is the ordered, ATP-costing shutdown of contraction: the motor neuron stops, ACh is broken down, Ca²⁺ is pumped back into the sarcoplasmic reticulum, and tropomyosin covers actin again.

Worked example — run the shutdown. You put the four relaxation steps in order.

The motor neuron stops firing.
ACh is broken down at the junction.
ATP-powered pumps return Ca²⁺ to the sarcoplasmic reticulum.
Tropomyosin covers actin's binding sites again, and the fiber relaxes.

The week's two clinical connections sit on this chain, named in standard terms. A receptor blocker at the junction leaves the muscle unable to contract, because step 1 of contraction cannot pass its signal into the fiber. Rigor mortis is the myosin heads locked to actin once ATP is gone. You name the structure each one involves, and you stop there.

Misconception check. Students often think relaxation needs no energy, because it feels like letting go. The cure is step 3: Ca²⁺ must be pumped back into the sarcoplasmic reticulum against its gradient, and that pump runs on ATP, the same way the Week 3 pumps did. Relaxation costs ATP.

8. Sort motor units and fiber types

Pick up a single grain of rice, then pick up a heavy backpack. The same hand handles both. Your nervous system controls muscle fibers in groups, and the fibers themselves come in different types.

A motor unit is one motor neuron plus every muscle fiber it supplies; small motor units give fine control. One motor neuron fires, and every fiber in its unit contracts.

Fibers also differ in how they get and spend energy. This is an overview, and it names two types:

A slow oxidative fiber is a skeletal muscle fiber rich in mitochondria, capillaries, and myoglobin that can contract for long periods without tiring, which suits it to holding posture.
A fast glycolytic fiber is a thick skeletal muscle fiber that stores much glycogen and contracts quickly and powerfully but tires fast.

Worked example — match the fiber to the job. You read three illustrative jobs and pick the better fiber type for each.

A distance runner's calf, working for a long time: slow oxidative, because those fibers resist fatigue.
A sprinter's calf in one explosive start: fast glycolytic, because those fibers contract quickly and powerfully.
The muscles that keep you sitting upright all afternoon: slow oxidative, because those fibers hold posture without tiring.

Misconception check. Students often think "fast" fibers are the better fibers. It is tempting because fast sounds strong. The cure is the trade: fast glycolytic fibers are quick and powerful but tire fast, while slow oxidative fibers are slower but keep going. Each type fits a different job.

9. Read fatigue on the grip-fatigue series

Go back to the tennis ball from the start of the chapter. Five rounds of squeezing, and the count drops each time. Now you can put numbers on it and read them through everything above.

Fatigue is a fall in a muscle's ability to keep contracting, reflecting ATP running low, lactic acid lowering the pH inside the fiber, and ion imbalances across the sarcolemma. Notice what is not on that list: the filaments do not get shorter or wear out.

To summarize a series, you will use one more term. The percent decline is the drop from the first value to the last, divided by the first value and multiplied by 100.

Worked example — Dataset G, the grip-fatigue series (illustrative counts constructed for this course, not one real person's data). Five 10-second all-out squeeze trials with 15-second rests gave 24, 21, 18, 15, and 12 squeezes. You add, average, find the drop and the percent decline, and read the trend.

Dataset G, the grip-fatigue series: illustrative squeezes per 10-second trial
Trial	1	2	3	4	5
Squeezes	24	21	18	15	12

Sum the trials: 24 + 21 + 18 + 15 + 12 = 90 squeezes.
Average the trials: 90 ÷ 5 = 18 squeezes per trial.
Total drop: first trial minus last trial, 24 − 12 = 12 squeezes.
Percent decline: the drop divided by the first trial, times 100: 12 ÷ 24 × 100 = 50%.
Trial-to-trial fall: 24 − 21 = 3, 21 − 18 = 3, 18 − 15 = 3, and 15 − 12 = 3, so the count falls by a steady 3 squeezes per trial.
Check the fall against the drop: 4 gaps × 3 squeezes = 12 squeezes, the same as the total drop.
Read the trend: ATP is spent faster than it is remade, and lactic acid lowers the pH inside the fiber, so fewer cross-bridges cycle in each trial; the filaments never shorten.

In words: by the fifth trial the hand made 12 versus 24 squeezes, half as many as in the first, a 50% decline, falling by the same 3 squeezes each round. A real hand would not fall this evenly; the series was built to land on clean numbers. Your own counts in this week's lab will differ, and that is fine. They are your own values, not a norm to meet.

Every one of those squeezes ran the same chain from Section 5: ACh at the neuromuscular junction → muscle action potential down the T-tubules → Ca²⁺ from the sarcoplasmic reticulum → Ca²⁺ binds troponin and tropomyosin uncovers actin → cross-bridge and power stroke (ATP). Fatigue does not change the order. It slows how many cross-bridges can keep cycling.

In practice (your tools). In Google Sheets or any free spreadsheet, type the five counts in cells B2 to B6. In B7, =SUM(B2:B6) gives the sum. In B8, =AVERAGE(B2:B6) gives the average. In B9, =B2-B6 gives the total drop. In B10, =(B2-B6)/B2*100 gives the percent decline. Check each result against the steps above before you trust it.

Honesty note: this week's lab asks you to squeeze until your hand slows. Stop at any pain. A toe-tap count or the pinned series above is always an acceptable substitute.

Pause and think, then choose one. (a) Describe a moment from your own week when a muscle slowed down after repeated work, and name which of the three causes of fatigue you think mattered most. (b) Describe a moment when a muscle held steady for a long time, and say which fiber type you think was doing the work.

Misconception check. Students often read a falling count as "the filaments got shorter" or "the muscle ran out of filaments." It is tempting because the muscle gives less each round. The cure: the filaments keep their length the whole time. What falls is how many cross-bridges cycle, because ATP runs low, lactic acid lowers the fiber's pH, and the ions drift out of balance.

Caveat: the three causes of fatigue are named here as an overview. How much each one matters varies with the task, and this course does not rank them.

Key terms

Fascicle — A bundle of muscle fibers inside a whole muscle, wrapped by the perimysium. (first used: 1. Climb down the hierarchy: from whole muscle to sarcomere)
Muscle fiber — One skeletal muscle cell, long and with many nuclei, whose membrane is the sarcolemma and whose cytoplasm is the sarcoplasm. (first used: 1. Climb down the hierarchy: from whole muscle to sarcomere)
Myofibril — A strand inside a muscle fiber made of sarcomeres, the level between the fiber and the sarcomere. (first used: 1. Climb down the hierarchy: from whole muscle to sarcomere)
Sarcomere — The functional unit of a myofibril, running from one Z disc to the next, where thin and thick filaments overlap and slide. (first used: 1. Climb down the hierarchy: from whole muscle to sarcomere)
Sarcolemma — The plasma membrane of a muscle fiber, along which the muscle action potential travels. (first used: 1. Climb down the hierarchy: from whole muscle to sarcomere)
Sarcoplasm — The cytoplasm of a muscle fiber. (first used: 1. Climb down the hierarchy: from whole muscle to sarcomere)
Epimysium — The connective-tissue wrapping around a whole skeletal muscle. (first used: 1. Climb down the hierarchy: from whole muscle to sarcomere)
Perimysium — The connective-tissue wrapping around each fascicle inside a muscle. (first used: 1. Climb down the hierarchy: from whole muscle to sarcomere)
Endomysium — The connective-tissue wrapping around each muscle fiber. (first used: 1. Climb down the hierarchy: from whole muscle to sarcomere)
Z disc — The boundary at each end of a sarcomere, where the thin filaments anchor; the Z discs move closer together when the sarcomere shortens. (first used: 2. Open a sarcomere: actin is thin, myosin is thick)
Thin filament — The filament anchored to the Z discs, made of actin and carrying the regulatory proteins troponin and tropomyosin. (first used: 2. Open a sarcomere: actin is thin, myosin is thick)
Actin — The protein of the thin filament, with binding sites that myosin heads grab during contraction. (first used: 2. Open a sarcomere: actin is thin, myosin is thick)
Thick filament — The filament in the middle of the sarcomere, made of myosin and carrying many heads. (first used: 2. Open a sarcomere: actin is thin, myosin is thick)
Myosin — The protein of the thick filament, whose heads attach to actin and pull it during contraction. (first used: 2. Open a sarcomere: actin is thin, myosin is thick)
Tropomyosin — A regulatory protein along the thin filament that covers actin's binding sites while the fiber is at rest. (first used: 2. Open a sarcomere: actin is thin, myosin is thick)
Troponin — A regulatory protein on the thin filament that binds Ca²⁺ and then moves tropomyosin off actin's binding sites. (first used: 2. Open a sarcomere: actin is thin, myosin is thick)
T-tubules — Passages that carry the muscle action potential from the sarcolemma deep into the muscle fiber. (first used: 3. Wire the fiber: T-tubules and the sarcoplasmic reticulum)
Sarcoplasmic reticulum — The membrane store inside a muscle fiber that holds Ca²⁺, releases it to start contraction, and takes it back with ATP-powered pumps. (first used: 3. Wire the fiber: T-tubules and the sarcoplasmic reticulum)
Sliding filament model — The classroom model of contraction in which thin filaments are pulled past thick filaments, so the sarcomere shortens while neither filament gets shorter. (first used: 4. Slide, do not shrink: the sliding filament model)
A band — The band of a sarcomere where the thick filaments lie; it keeps its width during contraction because the filaments do not shorten. (first used: 4. Slide, do not shrink: the sliding filament model)
Excitation-contraction coupling — The ordered chain of events that links a motor neuron's signal to the pull of the myosin heads: ACh release, the muscle action potential, Ca²⁺ release, Ca²⁺ binding troponin, and the power stroke. (first used: 5. Put contraction in order: excitation-contraction coupling)
Motor neuron — A nerve cell that carries a command to skeletal muscle fibers and releases acetylcholine at the neuromuscular junction. (first used: 5. Put contraction in order: excitation-contraction coupling)
Neuromuscular junction — The meeting point between a motor neuron's ending and a muscle fiber, where acetylcholine crosses the synaptic cleft to the motor end-plate. (first used: 5. Put contraction in order: excitation-contraction coupling)
Acetylcholine — The chemical messenger, written ACh, that a motor neuron releases at the neuromuscular junction to trigger the muscle fiber's own electrical signal. (first used: 5. Put contraction in order: excitation-contraction coupling)
Synaptic cleft — The narrow gap between a nerve ending and the cell it signals, which a chemical messenger crosses. (first used: 5. Put contraction in order: excitation-contraction coupling)
Motor end-plate — The region of the sarcolemma at the neuromuscular junction that receives acetylcholine. (first used: 5. Put contraction in order: excitation-contraction coupling)
Muscle action potential — The muscle fiber's own electrical signal, triggered by acetylcholine and carried along the sarcolemma and down the T-tubules. (first used: 5. Put contraction in order: excitation-contraction coupling)
Cross-bridge — The link formed when a myosin head attaches to a binding site on actin. (first used: 5. Put contraction in order: excitation-contraction coupling)
Power stroke — The pull of an attached myosin head that drags the thin filament toward the center of the sarcomere, using ATP. (first used: 5. Put contraction in order: excitation-contraction coupling)
Rigor mortis — The stiffness that follows death, because without ATP the myosin heads cannot release from actin. (first used: 6. Follow the fuel: ATP's three jobs)
Relaxation — The ordered, ATP-costing shutdown of contraction: the motor neuron stops, ACh is broken down, Ca²⁺ is pumped back into the sarcoplasmic reticulum, and tropomyosin covers actin again. (first used: 7. Run relaxation in order: an active shutdown)
Motor unit — One motor neuron plus every muscle fiber it supplies; small motor units give fine control. (first used: 8. Sort motor units and fiber types)
Slow oxidative fiber — A skeletal muscle fiber rich in mitochondria, capillaries, and myoglobin that can contract for long periods without tiring, which suits it to holding posture. (first used: 8. Sort motor units and fiber types)
Fast glycolytic fiber — A thick skeletal muscle fiber that stores much glycogen and contracts quickly and powerfully but tires fast. (first used: 8. Sort motor units and fiber types)
Fatigue — A fall in a muscle's ability to keep contracting, reflecting ATP running low, lactic acid lowering the pH inside the fiber, and ion imbalances across the sarcolemma. (first used: 9. Read fatigue on the grip-fatigue series)
Percent decline — The drop from the first value to the last, divided by the first value and multiplied by 100. (first used: 9. Read fatigue on the grip-fatigue series)

Summary

Muscle, fascicle, fiber, myofibril, sarcomere: big to small.
Epimysium, perimysium, endomysium: muscle, fascicle, fiber.
One muscle fiber is one long, multinucleate cell.
A sarcomere runs from one Z disc to the next.
Actin is thin and anchors to the Z discs; myosin is thick and carries the heads.
T-tubules carry the signal; the sarcoplasmic reticulum stores and releases Ca²⁺.
Filaments slide; they do not shorten, so the A band keeps its width.
Contraction order: ACh, muscle action potential, Ca²⁺ release, Ca²⁺ binds troponin, power stroke.
ATP pulls, releases the head, and pumps Ca²⁺ back.
No ATP means locked heads, which is rigor mortis.
Relaxation is active and costs ATP.
A motor unit is one motor neuron and all its fibers.
Slow oxidative fibers last; fast glycolytic fibers are quick but tire.
Fatigue means fewer cross-bridges cycling, never shorter filaments.

Check your understanding

Work these before looking at the answers — they are ungraded, and the answers (with reasoning) are at the bottom of the page.

In an illustrative series made up for this question, a person counts toe taps in five 10-second trials and gets 40, 36, 32, 28, and 24. Find the sum, the average, the total drop, and the percent decline.
A study card made up for this question lists the steps of a contraction as: Ca²⁺ binds troponin; ACh at the junction; Ca²⁺ released from the sarcoplasmic reticulum; power stroke; muscle action potential. Put them in order and say where the card's first step really belongs.
A classmate looks at a contracted sarcomere and says, "The A band stayed the same width, so this muscle did not really contract." Explain what is right and what is wrong about that statement.
In a made-up kitchen scene, a cook holds a heavy pot steady for a long time, then later snaps a towel in one quick flick. Which fiber type fits each job better, and why?

Answers (worked reasoning — read after attempting)

Sum: 40 + 36 + 32 + 28 + 24 = 160 taps. Average: 160 ÷ 5 = 32 taps per trial. Total drop: 40 − 24 = 16 taps. Percent decline: 16 ÷ 40 × 100 = 40%. The count fell by a steady 4 taps per trial, and 4 gaps × 4 taps = 16, which matches the drop. Read it as fewer cross-bridges cycling in each trial, not as shorter filaments.
The order is: ACh at the junction; muscle action potential; Ca²⁺ released from the sarcoplasmic reticulum; Ca²⁺ binds troponin; power stroke. The card's first step, Ca²⁺ binds troponin, belongs fourth. Calcium can bind troponin only after the signal has reached the fiber and the sarcoplasmic reticulum has released it.
What is right: the A band does keep its width during a contraction. What is wrong: that is exactly what a real contraction looks like. The A band is where the thick filaments lie, and the filaments do not shorten. The sarcomere shortens because the Z discs move closer as the thin filaments slide inward.
Holding the pot steady for a long time fits slow oxidative fibers, which are rich in mitochondria, capillaries, and myoglobin and keep working without tiring. The quick flick fits fast glycolytic fibers, which contract quickly and powerfully but tire fast.

Next up in this module: the lecture, the slides, the Readings & Resources page, the tutorial, the practice set, and the quiz. Next week the same pull becomes a lever model, as whole muscles team up across your joints.

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