Canonical Question

MSK – Muscle

V5 I1.i Historical V4 L1.i 2 appearances

Master answer

Anatomy

Skeletal Muscle	Smooth Muscle
Long, cylindrical, multi-nucleated cells	Spindle shaped single-nucleated cells
10 μm diameter 100 μm long	2 μm diameter 400 μm long
Striated	Not striated
Actin and Myosin arranged in sarcomeres	More actin than myosin Actin inserts into dense bodies and cell membrane
Well developed sarcoplasmic reticulum and transverse tubules	Poorly developed sarcoplasmic reticulum No Transverse tubules
Containes troponin in the thin filaments	Contains calmodulin → binds to Ca²⁺ → activates myosin light-chain kinase
Ca²⁺ released from cytoplasm from sarcoplasmic reticulum	Ca²⁺ enters cytoplasm from extracellulr fluid, sarcoplasmic reticulum and mitochondria
Cannot contract without nerve stimulation	Maintains tone in absence of nerve stimulation Visceral smooth muscle produces pacemaker potentials
Denervation results in muscle atrophy	denervation results in hypersensitivity to stimulation
Muscle fibers stimulated independently No gap junctions	Gap junctions usually present
Two Types 1. Extrafusal (α-motor neuron supply) a) Slow-type (tonic) b) Fast-type (twitch) – Slow fatigue (type 1/red – slow oxidative) – Fast fatigue-resistant (type 2B/red – fast oxidative) – Fast fatiguable (type 2B/white) 2. Intrafusal (γ-motor neuron supply) – Non-contractile sensory fibers associated with muscle spindles	Two types 1. Visceral – located in hollow viscera – linked in sheets by gap junctions – contractile elements extend across multiple cells – Spontaneous depolarisation 2. Multiunit – located in eye (iris and ciliary body), large blood vessels, small airways, hair follicles – No gap junctions – Under ANS control without spontanaetiy

Physiology

Skeletal Muscle	Smooth Muscle
Excitation
– Motor neuron depolarisation – ACh vesicular release – Multiple MEPs → End plate potential – Muscle AP propagates via T-tubles – Opens L-type Ca channels – Calcium induced calcium release from SR – Ca-troponin C interaction – Alteration and movement of Trop-tropomyocin complex – Exposure of Actin – Removal of Troponin I inhibition of myosin ATPase – Cross bridge cycling	– Motor neuron depolarisation – ACh vesicular release – Multiple MEPs → End plate potential – Muscle AP propagates – Opens L-type Ca channels
Contraction
Sliding filament cross bridge cycling – “Flexed” Myosin without ATP binds to Actin. – Binding of ATP to Myosin causes release of Actin/Myosin complex and extension of the head – In the presence of Ca, Actin binding sites are open and binding of myosin/Actin/ATP complex is formed – Hydrolysis of ATP to ADP + P in myosin head causes a conformational change “initial flexing” the myosin head and releasing phosphate – Release of ADP further flexes Myosin head – In presence of Ca return to step 2.	– Influx of EC Ca → ↑ IC [Ca] – Ca binds Calmodulin → Ca-Calmodulin complex – Ca-Calmod → ↑ MLCK activity → – Phosphorylation of Myosin Light chain (MLC) → Activation of Myosin ATPase – Normal Cross-bridge cycling as per Skeletal muscle cross bridge cycling – Latch-bridging (Sustained SM contraction with minimal O₂ or ATP use) ◦ ↓ IC [Ca] + dephosphorylation of MLC does not cause unbinding of actin/myosin ◦ Unbinding occurs slowly
Relaxation
– AChE metabolises ACh in the NMJ ◦ ↓ nAChR activation at MEP → ↓ EPP and muscle AP generation – SR actively sequesters Ca (via Ca-Mg ATPase) ◦ ↓ IC [Ca] → Ca removed from troponin C ◦ tropomyosin mediated inhibition of actin-myosin – Titin ◦ Elastic component of sarcomere → ↓ to normal length	– Ca removed from cell ◦ Ca ATPase ◦ Ca2+/Na+ antiport – Myosin Light Chain Phosphatase ◦ dephosphorylates MLC → inhibition of myosin ATPase

Gladwin / JC 2020

Answer by Gladwin, JC

Exam appearances

Exam	Exact wording	Relationship	Success
2015B Q11	Compare and contrast the anatomy and physiology of skeletal and smooth muscle.	historical_member	—
2024B Q04	Compare and contrast the anatomy and physiology of smooth and skeletal muscle.	historical_member	—