BIOSCI107 · Biology for Biomedical Science: Cellular Processes and Development
Cardiac & Smooth Muscle
Topic 7 (exam Section D) closes by contrasting the other two muscle types with skeletal muscle. Cardiac muscle has a plateau action potential, calcium-induced calcium release (CICR), gap-junction coupling, the SA-node pacemaker and Starling's law; smooth muscle uses a calmodulin–MLCK pathway with no troponin. The recurring exam task is the three-way comparison — how each is triggered, its Ca²⁺ source and its regulatory protein. Examined in the 40% final exam (paper Teleform MCQ).
What this chapter covers
- 01Cardiac structure: branched cells, intercalated discs = desmosomes (hold) + gap junctions (electrically couple → myogenic, coordinated beat)
- 02Ventricular action potential: phase 0 fast Na⁺, phase 2 plateau from L-type Ca²⁺ current, phase 3 K⁺ repolarisation; long refractory period → no tetanus
- 03Calcium-induced calcium release (CICR): L-type Ca²⁺ influx triggers SR ryanodine receptors to release more Ca²⁺
- 04SA-node pacemaker: unstable RMP, funny current (I_f) depolarisation → Ca²⁺-driven upstroke → K⁺ repolarisation; sets heart rate
- 05Autonomic control: vagus/ACh slows, sympathetic/noradrenaline speeds and strengthens; CO = SV × HR; Starling's law (more filling → more force)
- 06Smooth-muscle structure: no sarcomeres/striations, dense bodies, caveolae (no T-tubules), unitary (gap-junction-coupled) vs multiunit
- 07Smooth-muscle contraction: Ca²⁺ + calmodulin → MLCK → phosphorylates myosin light chain (myosin-based, no troponin); MLCP relaxes
- 08The three-way comparison (skeletal vs cardiac vs smooth): initiation, Ca²⁺ source, regulatory protein, sarcomeres, T-tubules
Contrasting the calcium trigger in the three muscle types
- +1(a) Skeletal: a voltage-driven muscle action potential travels down the T-tubules and directly opens SR Ca²⁺-release channels (the trigger is the voltage change from the Na⁺-driven AP). [+1]
- +1(a) Cardiac: the plateau AP lets Ca²⁺ enter through L-type (DHPR) channels, and that Ca²⁺ influx triggers the SR ryanodine receptors to release more Ca²⁺ — calcium-induced calcium release (CICR). Smooth: Ca²⁺ enters via voltage-dependent channels and the SR (via IP₃), from both extracellular and SR sources. [+1]
- +1(b) Regulatory protein: skeletal and cardiac both use troponin–tropomyosin (Ca²⁺ binds troponin on the thin filament). Smooth muscle has NO troponin — Ca²⁺ binds calmodulin, which activates myosin light-chain kinase (MLCK) to phosphorylate myosin; regulation is myosin-based. [+1]
- +1(c) Tetanus: skeletal muscle's action potential is brief and its refractory period short, so rapid stimulation lets twitches summate into fused tetanus. Cardiac muscle's action potential has a long plateau and therefore a long absolute refractory period that lasts almost the whole contraction — a second AP cannot fire until the muscle has largely relaxed, so twitches cannot summate. Each cardiac AP gives exactly one beat. [+1]
Key terms
- Calcium-induced calcium release (CICR)
- The cardiac excitation–contraction trigger: Ca²⁺ entering through sarcolemmal L-type (DHPR) channels during the action-potential plateau opens SR ryanodine receptors, releasing a larger store of Ca²⁺ that drives contraction. Contrast the skeletal trigger, which is the voltage change itself rather than incoming Ca²⁺.
- Cardiac plateau action potential
- The long ventricular action potential: phase 0 fast Na⁺ upstroke, phase 2 plateau sustained by an inward L-type Ca²⁺ current, phase 3 repolarisation as K⁺ channels open. Its length creates a long absolute refractory period, so cardiac muscle cannot summate twitches or tetanise — one action potential, one beat.
- Intercalated disc
- The junction between cardiac cells, combining desmosomes (which stop the cells pulling apart) and gap junctions (which electrically couple them so the heart contracts as a coordinated, myogenic unit rather than needing a nerve to each cell).
- SA node / pacemaker potential
- The heart's pacemaker: cells with an unstable resting potential that slowly depolarise (the funny current, I_f, carried by Na⁺) to threshold, then fire a Ca²⁺-driven upstroke, followed by K⁺ repolarisation. This sets the intrinsic heart rate, modulated by the autonomic nerves.
- Calmodulin–MLCK pathway
- Smooth-muscle contraction control, with no troponin: Ca²⁺ binds calmodulin, the Ca²⁺–calmodulin complex activates myosin light-chain kinase (MLCK), which phosphorylates the myosin light chain so myosin can cycle on actin. Myosin light-chain phosphatase (MLCP) dephosphorylates myosin to relax — regulation is myosin-based.
- Starling's law
- The intrinsic property that greater ventricular filling (preload/stretch) produces a more forceful contraction, so the heart pumps out what it receives. Cardiac output CO = stroke volume × heart rate; sympathetic noradrenaline further raises rate and force, vagal ACh lowers rate.
Cardiac & Smooth Muscle FAQ
How is the cardiac calcium trigger different from skeletal muscle?
In skeletal muscle the trigger is voltage: the muscle's own Na⁺-driven action potential travels down the T-tubules and mechanically opens the SR Ca²⁺-release channels — little external Ca²⁺ is needed. In cardiac muscle the trigger is Ca²⁺ itself: during the plateau, Ca²⁺ enters through L-type channels, and that incoming Ca²⁺ opens SR ryanodine receptors to release more — calcium-induced calcium release. Both then use troponin, but the way the SR is told to release Ca²⁺ differs, which is a classic exam contrast.
Why can't the heart go into tetanus?
Because its action potential is long. The cardiac plateau (sustained L-type Ca²⁺ current) stretches the action potential — and therefore the absolute refractory period — to last almost the entire contraction. A second action potential cannot fire until the muscle has largely relaxed, so twitches cannot summate into tetanus. This is protective: the heart must relax and refill between beats, so each action potential produces exactly one beat. Skeletal muscle, with a brief AP and short refractory period, can summate twitches into fused tetanus.
How does smooth muscle contract without troponin?
It regulates on the myosin side instead of the thin filament. Ca²⁺ (from voltage-dependent channels and the SR via IP₃) binds calmodulin; the Ca²⁺–calmodulin complex activates myosin light-chain kinase (MLCK), which phosphorylates the myosin light chain so myosin can cycle on actin — a slow, sustained contraction. Relaxation comes from myosin light-chain phosphatase (MLCP) removing that phosphate. This is why nitric oxide, which raises MLCP activity, relaxes smooth muscle and causes vasodilation.
Can AI help me with cardiac and smooth muscle in BIOSCI 107?
Yes, for study. Sia can build the three-way skeletal/cardiac/smooth comparison table with you, explain CICR versus the skeletal voltage trigger, and drill why the heart cannot tetanise. Use it to prepare for the final exam — it does not sit the exam for you, and the exam is an AI-free lane under the course's academic-integrity policy. Confirm the rules on Canvas.
Exam move
Everything in this chapter is best learned as a comparison against skeletal muscle, so build the master table the exam effectively asks for: for skeletal, cardiac and smooth, list initiation (neurogenic vs myogenic), Ca²⁺ source and trigger (voltage / CICR / IP₃ + influx), regulatory protein (troponin–tropomyosin for both striated types; calmodulin–MLCK for smooth), and whether there are sarcomeres and T-tubules. Attach the cardiac specials — the plateau AP and why it blocks tetanus, gap-junction coupling via intercalated discs, the SA-node pacemaker sequence, and Starling's law with CO = SV × HR — and the smooth-muscle specials (no striations, dense bodies, unitary vs multiunit, NO/MLCP relaxation). Rehearse the applied hooks (SERCA overexpression → stronger contraction; nitric oxide → vasodilation; cutting the nerve stops only skeletal muscle). This is exam material (Topic 7, Section D); confirm the exam date and Teleform format on Canvas.
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