Here are high-yield viva questions on Smooth Muscle & Cardiac Muscle — with model answers:
Viva Questions: Smooth Muscle & Cardiac Muscle
SMOOTH MUSCLE
Q1. Why does smooth muscle lack striations?
Smooth muscle has thick (myosin) and thin (actin) filaments, but they are not arranged into sarcomeres. Without the regular sarcomeric banding pattern, no cross-striations are visible under light microscopy.
Q2. What are the two types of smooth muscle? Give examples of each.
| Type | Examples |
|---|
| Unitary (single-unit) | GI tract, bladder, uterus, ureter |
| Multiunit | Iris, ciliary muscle of lens, vas deferens |
Unitary smooth muscle cells are linked by gap junctions → electrically coupled → coordinated contraction. Multiunit cells are independent, each densely innervated by the ANS.
Q3. What is the key difference in the mechanism of contraction between smooth muscle and skeletal muscle?
- Skeletal muscle: Ca²⁺ binds troponin C → removes tropomyosin inhibition → cross-bridge cycling
- Smooth muscle: No troponin. Ca²⁺ binds calmodulin → Ca²⁺-calmodulin activates myosin-light-chain kinase (MLCK) → MLCK phosphorylates myosin light chain → increases myosin ATPase → cross-bridge cycling
Q4. What are the three sources of Ca²⁺ for smooth muscle contraction?
- Voltage-gated Ca²⁺ channels (sarcolemma) — opened by depolarization
- Ligand-gated Ca²⁺ channels (sarcolemma) — opened by hormones/neurotransmitters via G proteins
- IP₃-gated SR channels — hormone → G protein → PLC → PIP₂ → IP₃ → Ca²⁺ release from SR
Key point: Unlike skeletal muscle (SR only), smooth muscle can raise [Ca²⁺] from both ECF and SR.
Q5. How does smooth muscle relax?
By falling [Ca²⁺] through:
- Hyperpolarization → closes voltage-gated Ca²⁺ channels
- cAMP/cGMP → inhibit Ca²⁺ channels or activate SR Ca²⁺-ATPase
- Reduced IP₃ production → less SR Ca²⁺ release
- Myosin-light-chain phosphatase → dephosphorylates myosin light chain → stops cross-bridge cycling
Q6. What are caveolae? What is their significance in smooth muscle?
Caveolae are shallow sarcolemmal invaginations (cholesterol/sphingolipid-rich lipid raft microdomains) that cluster near peripheral SR. They are the functional equivalent of T-tubules in smooth muscle — they facilitate coupling between membrane depolarization and SR Ca²⁺ release.
Q7. What is the role of calponin and caldesmon in smooth muscle?
At low [Ca²⁺]: calponin and caldesmon bind actin → inhibit myosin ATPase → prevent cross-bridge formation.
At high [Ca²⁺]: Ca²⁺-calmodulin → phosphorylation of calponin and caldesmon → inhibition is relieved → cross-bridges form.
Q8. What is pacemaker (slow wave) activity in smooth muscle?
Unitary smooth muscle shows spontaneous, rhythmic membrane depolarizations called slow waves, generated intrinsically by pacemaker cells (e.g., interstitial cells of Cajal in the GI tract). The frequency of slow waves determines the frequency of action potentials and therefore the rhythm of contractions.
CARDIAC MUSCLE
Q9. What is an intercalated disc? What structures does it contain and what is the function of each?
Intercalated discs are step-like junctions at the ends of cardiomyocytes where adjacent cells meet.
| Structure | Region | Function |
|---|
| Desmosomes | Transverse | Mechanical adhesion — withstands contractile forces |
| Fascia adherens | Transverse | Anchors actin filaments; strong intercellular adhesion |
| Gap junctions | Lateral/longitudinal | Ionic/electrical continuity — allows rapid impulse spread, functional syncytium |
Q10. Why is cardiac muscle called a functional syncytium?
Cardiac muscle cells are anatomically separate, but gap junctions in the intercalated discs allow free passage of ions between cells. An action potential in one cell propagates rapidly to adjacent cells, causing them to contract as a unit — behaving like a syncytium functionally, without being one structurally.
Q11. How does E-C coupling in cardiac muscle differ from skeletal muscle?
| Feature | Skeletal | Cardiac |
|---|
| Mechanism | Direct mechanical coupling (DHP receptor → RYR1) | CICR (Cav1.2 → Ca²⁺ entry → RYR2 → SR Ca²⁺ release) |
| Ca²⁺ source | SR only | ECF + SR |
| T-tubule location | A-I band junction | Z disc |
| SR junctions | Triads (2 terminal cisternae + 1 T-tubule) | Dyads (1 terminal cisterna + 1 T-tubule) |
| Ca²⁺ sensor | Troponin C | Troponin C |
Q12. Where are T-tubules located in cardiac muscle? What junction do they form?
T-tubules in ventricular cardiac muscle are located at the Z discs (not the A-I junction as in skeletal muscle). They associate with one terminal cisterna of SR, forming dyads (vs. triads in skeletal muscle).
Atrial cardiomyocytes have absent or very small T-tubules.
Q13. Why does cardiac muscle have so many mitochondria?
Mitochondria occupy up to 40% of cardiomyocyte volume — more than any other muscle type. The heart works continuously and relies almost exclusively on aerobic oxidative phosphorylation (primarily of fatty acids) for ATP. This high mitochondrial density reflects the enormous, uninterrupted energy demand.
Q14. What is atrial natriuretic factor (ANF)? Which cardiac cells secrete it?
ANF is a peptide hormone stored in secretory granules near the nuclei of atrial cardiomyocytes (~600 granules/cell in the right atrium). Released in response to atrial stretch (high blood volume) → acts on kidney → promotes Na⁺ and water excretion (natriuresis and diuresis) → reduces blood volume and pressure. It opposes aldosterone and ADH. This makes atrial muscle cells both contractile and endocrine in function.
Q15. Why does cardiac muscle have poor regenerative capacity?
Adult mammalian cardiomyocytes lack satellite cells (muscle stem cells). After injury (e.g., myocardial infarction), lost cardiomyocytes are replaced by fibrous scar tissue (fibrosis) rather than new muscle — this is the basis of post-MI remodeling and heart failure.
Q16. What is the difference between autorhythmicity and autonomic control of the heart?
- Autorhythmicity: The heart's rhythm is intrinsic — pacemaker nodes (SA node, AV node) generate spontaneous action potentials independently. Cardiac muscle cells in culture continue to beat.
- Autonomic control modulates but does not initiate the rhythm:
- Sympathetic → ↑ heart rate and contractility
- Parasympathetic → ↓ heart rate
HIGH-YIELD COMPARISON QUESTION
Q17. Compare smooth, cardiac, and skeletal muscle across key features.
| Feature | Skeletal | Cardiac | Smooth |
|---|
| Striations | Yes | Yes | No |
| Nuclei | Multiple, peripheral | Single, central | Single, central |
| Voluntary control | Yes | No | No |
| T-tubules | A-I junction (triads) | Z disc (dyads) | Caveolae |
| Ca²⁺ sensor | Troponin C | Troponin C | Calmodulin |
| Intercalated discs | No | Yes | No |
| Regeneration | Yes (satellite cells) | Minimal | Yes |
| Pacemaker activity | No | Yes | Unitary type: Yes |
| Endocrine function | No | Yes (ANF) | No |