DAT Review · Biology

Skeletal and Muscular Systems

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On this page 7 sections
  1. In 30 seconds
  2. The college version
  3. Eli explains
  4. Key takeaway
  5. Check yourself
  6. Study tools
  7. Sources & references

In 30 seconds

  • Bone cells: osteoblasts (build bone), osteoclasts (break down bone), osteocytes (mature bone cells in lacunae). Calcium homeostasis controlled by PTH (increases blood Ca²⁺) and calcitonin (decreases blood Ca²⁺).
  • Three muscle types: skeletal (voluntary, striated, multinucleated), smooth (involuntary, non-striated, single nucleus), cardiac (involuntary, striated, intercalated discs).
  • Sarcomere structure: actin (thin) and myosin (thick) filaments, Z-lines as boundaries. ATP is required for myosin head detachment — rigor mortis results from ATP depletion.

The college version

Core Review

The Skeletal System

Functions of bone: Support and structural framework, protection of vital organs (skull protects brain, rib cage protects heart/lungs), movement (attachment points for muscles), mineral storage (calcium and phosphate), blood cell production (hematopoiesis in red bone marrow), and energy storage (yellow bone marrow stores fat).

Bone Structure:

  • Compact bone: Dense outer layer composed of osteons (Haversian systems) — concentric rings (lamellae) of mineralized matrix around a central Haversian canal containing blood vessels and nerves. Osteocytes sit in lacunae, connected by canaliculi for nutrient exchange.
  • Spongy (cancellous) bone: Lighter interior with a honeycomb structure of trabeculae. Found in the epiphyses of long bones and flat bones. Contains red bone marrow for hematopoiesis.

Bone Cells:

  • Osteoblasts: Build bone by secreting collagen and mineralizing the matrix. Found on bone surfaces.
  • Osteoclasts: Large, multinucleated cells derived from monocytes/macrophages. They secrete acid and enzymes to resorb (break down) bone matrix, releasing Ca²⁺ into the blood.
  • Osteocytes: Mature osteoblasts that become trapped within the mineralized matrix. They reside in lacunae and sense mechanical stress, signaling for remodeling.

Axial vs. Appendicular Skeleton:

  • Axial: Skull, vertebral column, ribs, sternum (80 bones). Protects CNS and thoracic organs.
  • Appendicular: Pectoral and pelvic girdles, limbs (126 bones). Enables locomotion and manipulation.

Calcium Homeostasis: Blood Ca²⁺ must be maintained within a narrow range (~9–10.5 mg/dL). Two hormones regulate this:

  • Parathyroid hormone (PTH): Released by the parathyroid glands when blood Ca²⁺ is LOW. PTH stimulates osteoclast activity (bone resorption), increases kidney Ca²⁺ reabsorption, and activates vitamin D (which increases intestinal Ca²⁺ absorption). Net effect: increases blood Ca²⁺.
  • Calcitonin: Released by the thyroid gland when blood Ca²⁺ is HIGH. It inhibits osteoclast activity and stimulates osteoblasts (bone deposition). Net effect: decreases blood Ca²⁺. (Calcitonin is less critical in adult humans; PTH is the dominant calcium regulator.)

The Muscular System

Three Types of Muscle:

FeatureSkeletalSmoothCardiac
ControlVoluntaryInvoluntaryInvoluntary
StriationsYesNoYes
NucleiMultinucleatedSingle, central1–2, central
LocationAttached to bonesWalls of hollow organs, blood vesselsHeart (myocardium)
Special featuresSarcomeresNo sarcomeres; calmodulin-mediatedIntercalated discs (gap junctions + desmosomes); autorhythmic
Speed of contractionFastSlowModerate

Skeletal Muscle Organization: Muscle → fascicles → muscle fibers (cells) → myofibrils → sarcomeres. The sarcolemma (plasma membrane) has invaginations called T-tubules (transverse tubules) that propagate action potentials deep into the fiber. The sarcoplasmic reticulum (specialized smooth ER) stores and releases Ca²⁺.

The Sarcomere and Sliding Filament Mechanism: The sarcomere is the functional contractile unit, bounded by Z-lines. It contains:

  • Thin filaments (actin): Anchored at Z-lines. Include tropomyosin (blocks myosin binding sites in resting muscle) and troponin (Ca²⁺-binding complex).
  • Thick filaments (myosin): Contain myosin heads with ATPase activity that bind actin and perform the power stroke.

Steps of Muscle Contraction:

  1. Action potential arrives at the neuromuscular junction, releasing acetylcholine (ACh), which depolarizes the sarcolemma.
  2. Depolarization travels down T-tubules, triggering Ca²⁺ release from the sarcoplasmic reticulum.
  3. Ca²⁺ binds troponin, causing a conformational change that moves tropomyosin, exposing myosin-binding sites on actin.
  4. Myosin head (already "cocked" with ADP + Pᵢ from prior ATP hydrolysis) binds actin, forming a cross-bridge.
  5. Power stroke: Myosin head pivots, pulling actin filament toward the M-line (center of the sarcomere). ADP and Pᵢ are released.
  6. ATP binds to the myosin head, causing it to detach from actin.
  7. ATP is hydrolyzed to ADP + Pᵢ, re-cocking the myosin head. The cycle repeats as long as Ca²⁺ remains elevated and ATP is available.
  8. When the action potential ends, Ca²⁺ is actively pumped back into the sarcoplasmic reticulum, tropomyosin re-covers myosin-binding sites, and the muscle relaxes.

Rigor mortis: After death, ATP production ceases. Without ATP, myosin heads cannot detach from actin, locking muscles in a contracted state. This resolves as proteins degrade several hours later.

Common Traps

  • "Calcitonin is the most important calcium regulator": No — PTH is. Calcitonin plays a minor role in humans. The DAT may ask what hormone is released in response to HIGH Ca²⁺, which IS calcitonin, but PTH is the primary regulator overall.
  • "Smooth muscle has sarcomeres": No. Smooth muscle contracts via a different mechanism (calmodulin → myosin light-chain kinase → phosphorylation). Sarcomeres are unique to skeletal and cardiac muscle.
  • "ATP causes muscle contraction": This is backwards. ATP causes RELAXATION (allows myosin to detach from actin). ATP hydrolysis provides the energy for contraction (cocking the myosin head), but ATP binding is the detachment step.
Eli, the EliExplains learning guide

Eli explains

The same idea, in plain words

Explain it like I’m 10

Your skeleton is like the steel frame of a building — it holds you up, protects your organs, and stores calcium like a bank stores money. When your blood is low on calcium (you need it for nerves and muscles), PTH acts like a bank withdrawal slip: it tells osteoclasts (demolition crew) to break down some bone and release calcium. When there's too much, calcitonin tells the builders (osteoblasts) to put some calcium back.

Muscles work like a tug-of-war rope with pulling arms (myosin heads) grabbing two parallel ropes (actin filaments) and pulling them together. The arms can only grab when calcium clears the way (by moving tropomyosin out of the way). To let go and re-grab higher up, each arm needs an ATP "energy token." Without ATP (rigor mortis), the arms stay locked on — like a game of tug-of-war where the referee died and nobody can let go.

Key takeaways

  • Osteoblast vs. osteoclast: Build vs. break down. PTH activates osteoclasts. Know the sequence and direction.
  • Haversian system (osteon): Central canal → lamellae → lacunae (osteocytes) → canaliculi. Compact bone only.
  • Sarcomere bands: During contraction, the H zone and I band shorten; the A band (length of thick filaments) remains the same. Z-lines move closer together.
  • ATP roles in contraction: (1) Detach myosin from actin, (2) Re-cock the myosin head (hydrolysis), (3) Pump Ca²⁺ back into SR (active transport).
  • Intercalated discs in cardiac muscle contain gap junctions (electrical coupling) and desmosomes (mechanical adhesion).

Check yourself

3 review questions from the chapter. Try each one, then open the answer.

  1. A patient has a parathyroid tumor causing excess PTH secretion. What happens to blood calcium levels and bone density?

    Show answer

    Blood calcium would be elevated (hypercalcemia). Excess PTH stimulates osteoclast activity, causing bone resorption that releases Ca²⁺ into the blood. Bone density would decrease (osteoporosis-like effects) as bone is broken down faster than it's rebuilt. Renal Ca²⁺ reabsorption and vitamin D activation would also increase.

  2. During skeletal muscle contraction, which bands/zones of the sarcomere shorten, and which stays the same length?

    Show answer

    The I band (region containing only thin filaments) and H zone (region containing only thick filaments) shorten. The A band (length of the thick filaments) stays the same. The Z-lines move closer together as the sarcomere contracts.

  3. How does cardiac muscle differ from skeletal muscle in terms of both structure and control?

    Show answer

    Structurally, cardiac muscle is striated but has 1-2 centrally located nuclei (vs. multinucleated skeletal), and is connected by intercalated discs containing gap junctions (electrical coupling) and desmosomes. Functionally, cardiac muscle is involuntary and autorhythmic — it generates its own action potentials via pacemaker cells (SA node) without neural input. Skeletal muscle is voluntary and requires neural stimulation at the neuromuscular junction to contract.

Keep learning

Ready to build on this? Continue to the next lesson.

Study tools & related lessonsYou’ll learn to · Related

You’ll learn to

  • Describe the functions of bone and distinguish between compact and spongy bone.
  • Compare the roles of osteoblasts, osteoclasts, and osteocytes in bone remodeling and calcium homeostasis.
  • Differentiate the three muscle types histologically and functionally.
  • Explain the sliding filament mechanism of muscle contraction, including the roles of Ca²⁺, troponin, tropomyosin, and ATP.

Sources & references

  1. OpenStax Biology 2e, Chapter 38: "The Musculoskeletal System"
  2. NCBI Bookshelf, Molecular Biology of the Cell, 4th edition, Chapter 16: "The Cytoskeleton" (includes muscle contraction)
  3. NIH Osteoporosis and Related Bone Diseases National Resource Center: "What Is Bone?"

This lesson was adapted from the open educational references above; their licenses and attributions are preserved. See Copyright & Licensing.

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