Compare the three muscle tissue types, explain contraction by the sliding filament theory, describe muscle fatigue and energy use, and identify major muscles and their actions

Learning goal: Compare skeletal, cardiac and smooth muscle cells by structure, location and control; explain how an action potential leads to contraction of sarcomeres as described by the sliding filament theory; describe how muscles use energy, respond to stimuli, fatigue and grow with exercise; identify the major muscles of the head, face and neck, the trunk and the upper and lower limbs and the movements they produce with the skeleton; describe the connective tissues that organize a muscle; and explain homeostatic imbalances including muscular dystrophy, atrophy and the effects of steroids.

What muscle does. The muscular system consists of three types of muscle cells: skeletal, smooth and cardiac. Their shared property is contraction: when stimulated, the cell shortens or develops tension. Through contraction, muscle moves the body and the fluids inside it, maintains posture against gravity, stabilizes joints by keeping tension on them and generates heat, which is why shivering warms you and why exercise heats the body quickly; at rest, organs such as the liver, brain and heart produce a large share of body heat as well. Muscles are controlled voluntarily, through conscious commands, or involuntarily, by parts of the nervous system that run without awareness, or by both, as breathing muscles are.

Three cell types compared. Skeletal muscle cells, called fibers, are found attached to bones and, in the face, to skin. They are long cylinders, multinucleated, and striated, striped under the microscope because their contractile proteins line up in register; they are under voluntary control. Cardiac muscle cells, in the heart wall only, are shorter and branched, striated, usually with one nucleus, and joined end to end by intercalated discs, junctions that hold cells together and let the electrical signal pass directly from one cell to the next so the muscle of the atria, and then of the ventricles, contracts as a coordinated unit; control is involuntary and the heart sets its own rhythm. Smooth muscle cells, in the walls of hollow organs and blood vessels, are spindle-shaped, with one central nucleus and no striations, because their contractile proteins are arranged diagonally; they contract slowly, can stay contracted for long periods with little energy, and are involuntary.

How a skeletal muscle is organized. A whole muscle is wrapped in a sheet of dense connective tissue, the epimysium, which continues at each end as a tendon (dense regular connective tissue) that anchors the muscle to bone. Inside, bundles of fibers called fascicles are wrapped in perimysium, and each fiber is wrapped in a delicate endomysium. These three connective tissue layers carry blood vessels and nerves and transmit the force of contraction to the tendon; the connective tissues of the body, loose, dense, cartilage, bone and blood, were described in the tissue lesson, and dense regular tissue is the one that muscle depends on. Inside each fiber run hundreds of myofibrils, and each myofibril is a chain of repeating units called sarcomeres. A sarcomere runs from one Z disc to the next. Thin filaments of the protein actin, with two regulatory proteins, tropomyosin and troponin, wound along them, are anchored to the Z discs and point toward the center. Thick filaments of myosin lie in the center, overlapping the ends of the thin filaments; each myosin molecule has a head that can bind actin. The striations are the pattern of overlap: the dark A band is the length of the thick filaments, the light I band contains only thin filaments, and the H zone in the middle of the A band contains only thick filaments.

From nerve impulse to contraction. A motor neuron carries an action potential to the neuromuscular junction, where its ending releases the neurotransmitter acetylcholine. Acetylcholine binds receptors on the fiber's membrane and triggers an action potential in the muscle fiber, which spreads over the surface and inward along tubes called T tubules. The T tubules signal the sarcoplasmic reticulum, a membrane network around each myofibril, to release stored calcium ions into the cytoplasm. Calcium binds troponin, which pulls tropomyosin aside and exposes the myosin-binding sites on actin. Now the sliding filament cycle runs. A myosin head, already energized by splitting ATP into ADP and phosphate, binds actin, forming a cross-bridge. The head pivots, the power stroke, releasing the ADP and phosphate and pulling the thin filament toward the sarcomere's center. A new ATP binds the head, which releases actin. The head splits that ATP and returns to its energized position, ready to bind again farther along. With thousands of heads cycling out of step, the thin filaments slide inward along the thick ones; the Z discs approach each other, the I band and H zone narrow, but the A band stays the same length because the filaments themselves do not shorten. They slide. Every sarcomere shortening a little makes the whole fiber shorten. Relaxation happens when the neuron stops firing: an enzyme breaks down acetylcholine, calcium is pumped back into the sarcoplasmic reticulum using ATP, troponin releases its calcium, tropomyosin covers the sites again and the heads can no longer bind. Within the cross-bridge cycle ATP has two roles, releasing the myosin head from actin and re-cocking it; outside the cycle it also powers the calcium pump. ATP is therefore needed both to contract and to relax; after death, with no ATP, heads stay locked on actin and the body stiffens.

Energy and responses to stimuli. A fiber stores only a few seconds of ATP. The three ways of re-forming it overlap, but each dominates at a different time scale. In the first roughly fifteen seconds of intense work, creatine phosphate donates its phosphate to ADP to re-form ATP instantly. In efforts lasting up to about a minute, glycolysis breaks glucose down without oxygen, yielding a little ATP quickly and producing lactate. For sustained activity, aerobic respiration in the mitochondria supplies most of the ATP, using oxygen delivered by the blood and fuel from glucose, glycogen and fatty acids, and it is why breathing and heart rate rise during exercise. A single stimulus produces a twitch; stimuli arriving faster than the fiber can relax add together, and at high frequency produce a smooth sustained contraction called tetanus, which is how most ordinary voluntary movements are produced. Force is graded by the number of motor units, a motor neuron and all the fibers it controls, that are recruited: a few for lifting a pencil, most for lifting a chair.

Muscle fatigue. Fatigue is the decline in a muscle's ability to produce force during continued stimulation. Its physiology is not simply lactic acid, an older idea that the evidence does not support. In intense activity, phosphate and hydrogen ions accumulate inside the fiber and interfere with calcium release and with the cross-bridge cycle; creatine phosphate and glycogen run down; potassium leaking out of the fiber disturbs its excitability; and in long efforts the nervous system's drive to the muscle also falls. The result is that each stimulus produces less force until rest restores the fiber. An example: squeezing a clothespin as fast as possible, the count per twenty seconds falls steadily over two minutes and recovers after a rest.

Major muscles and their actions. Muscles are studied by group. Head, face and neck: the frontalis raises the eyebrows; the orbicularis oculi closes the eye and the orbicularis oris closes the lips; the masseter and temporalis close the jaw for chewing; the sternocleidomastoid, one on each side of the neck, flexes the head or turns it to the opposite side; the trapezius extends the head and lifts the shoulders. Trunk: the pectoralis major pulls the arm forward and across; the latissimus dorsi pulls the arm down and back; the deltoid caps the shoulder and abducts the arm; the rectus abdominis flexes the trunk; the external oblique twists it; the erector spinae along the spine extend the back and hold it upright; the diaphragm and intercostals drive breathing. Upper limb: the biceps brachii flexes the elbow and supinates the forearm; the brachialis beneath it flexes the elbow; the triceps brachii extends the elbow; forearm flexors and extensors move the wrist and fingers. Lower limb: the gluteus maximus extends the hip, as in climbing stairs; the quadriceps femoris on the front of the thigh (rectus femoris and three vastus muscles) extends the knee; the hamstrings on the back of the thigh (biceps femoris, semitendinosus, semimembranosus) flex the knee and extend the hip; the adductors pull the thigh inward; the tibialis anterior dorsiflexes the foot; the gastrocnemius and soleus of the calf plantar flex it through the calcaneal (Achilles) tendon. By convention a muscle's origin is its attachment to the bone that usually stays still, and its insertion is on the bone that usually moves; in some actions, such as a pull-up, the roles reverse, but the names stay the same. Because muscles only pull, they work in opposing pairs across a joint: the prime mover produces the movement, its antagonist produces the opposite movement and relaxes or brakes during it, and synergists assist. The biceps and triceps at the elbow, and the quadriceps and hamstrings at the knee, are the standard examples.

Exercise, steroids and imbalances. Resistance exercise makes fibers build more myofibrils, so each fiber thickens; this hypertrophy is how muscle is built, because the number of fibers scarcely changes. Endurance exercise adds mitochondria and capillaries instead. Anabolic steroids are synthetic relatives of the hormone testosterone that increase protein synthesis in muscle; they have medical uses, such as replacing missing hormone or treating muscle wasting, but taken to enhance performance they carry risks including liver damage, heart and blood vessel disease, disturbed mood, suppression of the body's own hormone production and, in adolescents, early closure of the epiphyseal plates that stops growth; they are banned in organized sport. Muscular dystrophy is a group of inherited diseases in which fibers break down; in Duchenne muscular dystrophy, an X-linked disorder, a protein called dystrophin that anchors the contractile machinery to the fiber's membrane is missing, so fibers tear during contraction and are gradually replaced by fat and connective tissue, with progressive weakness. Atrophy is loss of muscle mass when fibers are unused, as in a limb in a cast, when their nerve supply is cut, or with aging; in disuse atrophy the fibers shrink rather than disappear, so renewed use rebuilds them; after long loss of the nerve supply, fibers can be lost for good. These explanations are physiology, not medical advice.

Investigation: muscle fatigue with a clothespin. Hold a spring clothespin between thumb and index finger and squeeze it fully open and closed as fast as possible while a partner counts squeezes in each twenty-second interval for two minutes. Rest five minutes and repeat with the other hand. Record all six counts for each hand and plot count against time. A falling count over the two minutes supports the claim that repeated stimulation reduces force output; comparing dominant and non-dominant hands, and pooling class data by handedness, sex and height, shows whether these factors relate to the rate of decline, though a class sample is small. The investigation shows fatigue as a behavior; it cannot show the phosphate, calcium or glycogen changes inside the fibers that cause it, and motivation and pain tolerance affect the counts.

Worked identification of muscle tissue from micrographs: Micrograph 1: long parallel fibers, many nuclei at the edge, clear cross-striations. Micrograph 2: branching cells with striations, single central nuclei and dark stepped lines between cells. Micrograph 3: tapered cells with one elongated central nucleus and no striations, packed in sheets. Micrograph 1 is skeletal muscle from a limb or trunk muscle; micrograph 2 is cardiac muscle, the stepped lines being intercalated discs; micrograph 3 is smooth muscle from a vessel or organ wall. Striations go with fast contraction (1 and 2), branching with discs with contraction as a unit (2), and tapered unstriated cells with slow sustained contraction (3).

Worked sliding filament sequence with a model: Build the model from household items: two rulers for the Z discs, drinking straws taped to each ruler as thin filaments pointing inward, a pencil lying between them as the thick filament with paper-clip hooks for myosin heads. Step 1, an action potential arrives and calcium is released: turn over a card marked calcium. Step 2, calcium binds troponin and tropomyosin moves: remove the paper strips covering the straws. Step 3, hooks grip the straws (cross-bridges form). Step 4, hooks pivot toward the pencil's middle, pulling the rulers closer (power stroke). Step 5, add an ATP token; the hooks release. Step 6, split the token; the hooks re-cock and grip farther along. Repeating steps 3 to 6 brings the rulers together: the sarcomere shortens while the straws and pencil keep their lengths. The model shows sliding, the role of calcium and the role of ATP; it cannot show the thousands of heads cycling out of step, the true sizes or the speed.

Worked antagonistic pair and comparison of contraction length: Bending the elbow in a palm-up curl: the biceps brachii (origin on the scapula, insertion on the radius) is the prime mover for flexion; the triceps brachii (origins on the scapula and humerus, insertion on the olecranon of the ulna) is the antagonist and relaxes; the brachialis, a strong flexor in every forearm position, and the brachioradialis assist as synergists. Straightening the elbow reverses the roles. To compare contraction, measure the elbow angle at full flexion and full extension with a protractor and mark two skin points over each muscle belly to track the change in distance between them; the biceps shortens visibly during flexion while the triceps lengthens, and the reverse during extension. Force comparison requires a spring scale pulled first by flexing and then by extending against it; typically flexion is stronger at the elbow because of leverage and muscle size.

Worked fatigue data: Hypothetical clothespin counts per twenty seconds, dominant hand: 48, 41, 35, 30, 27, 25. The count falls by 23 squeezes, almost half, over two minutes; the fastest decline is in the first minute, consistent with the running down of creatine phosphate and the build-up of phosphate and hydrogen ions before aerobic supply catches up. The non-dominant hand: 44, 36, 30, 25, 23, 21, a similar pattern from a lower start. The data show the behavior of fatigue; they do not measure its chemical causes.

Representation task: Create a presentation or poster that describes and differentiates the three muscle tissue types (shape, nuclei, striations, intercalated discs, location, control) and includes a labeled sarcomere before and after contraction showing which bands change and which do not. On an outline of the body, label twelve major muscles, three from each group (head, face and neck; trunk; upper limb; lower limb), with the movement each produces.

Independent performance: Carry out the clothespin fatigue investigation and build the sliding filament model, then write a report. Success criteria: (a) counts per twenty-second interval for two minutes are recorded for both hands of at least three people, graphed and described, with the rate of decline compared by handedness and one other factor; (b) the physiology of fatigue is explained without attributing it simply to lactic acid; (c) the model demonstrates, in order, calcium release, exposure of binding sites, cross-bridge formation, the power stroke, ATP-driven release and re-cocking, and the report names two things the model cannot show; (d) one antagonistic pair is identified with origin, insertion, prime mover and antagonist for one movement; (e) muscular dystrophy or atrophy is explained by the structure that fails, and one effect and one risk of anabolic steroids are stated.