PSIO 201

Exam 3

What are the specific functions of skeletal muscle?

Movement of the body, maintenance of posture, stabilization of joints, heat generation, protection of internal organs, and control of body openings/exits. (3.1)

Define origin and insertion of a muscle.

Origin: The fixed attachment point of a muscle. Insertion: The movable attachment point of a muscle. (3.1)

What is the reverse action of a muscle?

When the insertion is fixed and the origin moves toward the insertion during contraction. (3.1)

List the three classes of levers in the body and their characteristics.

First-class: Fulcrum between effort and load (e.g., neck extension). Can favor force or speed. Second-class: Load between fulcrum and effort (e.g., plantar flexion). Favors force. Third-class: Effort between fulcrum and load (e.g., biceps brachii flexion). Favors speed and range of motion. (3.1)

Define agonist, antagonist, synergist, and fixator.

Agonist: Primary mover. Antagonist: Opposes the movement. Synergist: Assists the agonist. Fixator: Stabilizes origin of agonist. (3.1)

Describe the role of myoblasts and satellite cells in muscle development.

Myoblasts: Embryonic precursors that fuse to form multinucleated muscle fibers. Satellite cells: Adult stem cells that repair and grow muscle fibers. (3.2)

Difference between hyperplasia and hypertrophy.

Hyperplasia: Increase in muscle fiber number (rare in humans). Hypertrophy: Increase in muscle fiber size via more myofibrils and sarcomeres. (3.2)

What is the function of connective tissue in skeletal muscle?

Supports muscle structure, transmits force, protects fibers, organizes fascicles, and links muscle to bone (via tendons). Includes epimysium, perimysium, endomysium, and fascia. (3.2)

What proteins make up the sarcomere and their roles?

Thin filament: Actin, troponin (regulates Ca²⁺ binding), tropomyosin (blocks myosin binding). Thick filament: Myosin (crossbridge formation, power stroke). Structural proteins: Titin (elasticity), nebulin (aligns actin), myomesin (M-line), dystrophin (connects filaments to sarcolemma). (3.2)

Describe the sliding filament model.

Actin slides past myosin during contraction; sarcomere shortens. A band stays same, I band and H zone shorten. (3.2)

Define a crossbridge.

The connection formed when a myosin head binds to an actin filament during contraction. (3.3)

Steps of the crossbridge cycle.

1. Crossbridge formation: Myosin binds actin. 2. Power stroke: Myosin head pivots, sliding actin. 3. Detachment: ATP binds myosin, releasing actin. 4. Reactivation: ATP hydrolysis resets myosin head. (3.3)

Role of calcium and troponin in contraction.

Calcium binds troponin, moving tropomyosin off actin’s binding site, allowing crossbridge formation. (3.3)

Explain rigor complex and rigor mortis.

Rigor complex: Myosin tightly bound to actin after power stroke without ATP. Rigor mortis occurs postmortem because ATP is depleted, preventing crossbridge detachment. (3.3)

What is a motor unit?

A single motor neuron and all the muscle fibers it innervates. (3.4)

Events at the neuromuscular junction.

1. Action potential reaches synaptic end bulb. 2. Ca²⁺ enters, triggering ACh release. 3. ACh binds receptors on motor end plate. 4. Na⁺ influx generates muscle action potential. 5. AChE breaks down ACh, ending signal. (3.4)

Role of calcium in contraction and relaxation.

Calcium binds troponin to enable contraction; pumped back into SR via Ca²⁺ ATPase to relax muscle. (3.4)

ATP sources for muscle contraction.

Creatine phosphate (~10 sec), Glycolysis (~1–2 min, anaerobic), Aerobic metabolism (hours). (3.5)

Define fatigue and oxygen debt.

Fatigue: Inability to maintain tension due to substrate depletion or metabolite accumulation. Oxygen debt: Extra O₂ consumed post-exercise to restore ATP, CP, and remove lactate. (3.5)

Three phases of a muscle twitch.

Latent: AP spreads, Ca²⁺ release starts. Contraction: Crossbridges form, tension rises. Relaxation: Ca²⁺ reabsorbed, tension falls. (3.6)

Compare twitch vs tetanus.

Twitch: Single AP causes single contraction. Tetanus: High-frequency APs sum to sustained contraction (temporal summation). (3.6)

Strategies to increase force.

Spatial summation: Recruit more motor units. Temporal summation: Increase stimulation frequency. Optimal sarcomere length. (3.6)

Compare isometric, concentric, eccentric contractions.

Isometric: Tension, no shortening. Concentric: Shortening under tension. Eccentric: Lengthening under tension. (3.6)

Muscle fiber types: SO, FOG, FG.

SO (Type I): Slow, oxidative, endurance, high myoglobin. FOG (Type IIA): Fast, mixed oxidative-glycolytic, moderate endurance and power. FG (Type IIX): Fast glycolytic, high power, low endurance. (3.7)

Hybrid vs pure fibers.

Hybrid fibers express multiple myosin types; adapt with training to specialize. Pure fibers express only one type. (3.7)

Role of myoglobin.

Oxygen-binding protein in muscle, high in SO fibers, gives red color. (3.7)

Hypertrophy vs atrophy.

Hypertrophy: Fiber size increases (more myofibrils). Atrophy: Fiber size decreases from disuse or aging. (3.7)

Role of satellite cells.

Repair damaged fibers by donating nuclei, enabling new protein synthesis. (3.7)

Compare cardiac vs skeletal muscle structure.

Cardiac: Branched, 1–2 nuclei, intercalated discs (desmosomes + gap junctions). Skeletal: Long, multinucleate, no discs. Both have sarcomeres. (3.8)

Cardiac vs skeletal contraction differences.

Cardiac: Autorhythmic, single twitch, slower AP, no motor units, involuntary (ANS). Skeletal: Voluntary, motor units, fast twitch, can tetanize. (3.8)

Smooth vs skeletal muscle function.

Smooth: Involuntary, controls tube diameter, slower, can be single/multiunit, uses actin/myosin overlap. Skeletal: Voluntary, locomotion/posture, fast, striated. (3.8)

Smooth muscle structure.

Spindle-shaped cells, non-striated, thick/thin filaments loosely organized, autorhythmic, influenced by ANS. (3.8)