L1i / 15B11: Compare and contrast the anatomy and physiology of skeletal muscle and smooth muscle

15B11: Exam Report

Compare and contrast the anatomy and physiology of skeletal and smooth muscle.

23% of candidates passed this question.

It was expected answers would describe in detail the role of troponin, tropomyosin and calmodulin in mediating muscle contraction. Detail on the structure (histology) of the skeletal and smooth muscle cells was often lacking. Many answers omitted the mechanism of muscle relaxation.

L1i / 15B11: Compare and contrast the anatomy and physiology of skeletal muscle and smooth muscle


Skeletal Muscle

Striated muscle tissue which is under voluntary control of the somatic nervous system

Smooth Muscle

Involuntary non-striated muscle


Skeletal Muscle


Smooth Muscle

Walls of vessels, organs: resp tract, skin, walls of hollow organs; uterus, stomach, intestines, bladder


Skeletal Muscle

Motor unit = nerve ending + muscle fibres

Each fibre 10-100mm diam

Striated, ordered sarcomeres

Smooth Muscle

No striations = looks smooth

 30-200mm LENGTH →thousands of times shorter than Sk m!


Skeletal Muscle

Multiple parallel myofibrils


Mitochondria (aerobic & anaerobic metabolism)

SR (Ca++ storage)

Glycogen (E storage)

Myoglobin (O2 storage)

Smooth Muscle

One nucleus per cell

No striations → myosin and actin is disordered

No troponin



Skeletal Muscle

Sarcomere = functional unit


Contractile proteins = actin & myosin

  • Myosin = heavy protein, long tail w 2 heads
  • Actin = thin protein in double strands

Regulatory proteins = Tropomysin & Troponin

  • Troponin: protein w 3 subunits

I – inhibits myosin ATPase

C- binds Ca++

T- binds Tropomysin

  • Tropomysin – blocks actin/myosin interaction

Smooth Muscle


Wandering membrane potential & resting tone


Requires extracellular  Ca++

For excitation-contraction-coupling

SR is poorly developed

Contractile proteins = Actin & Myosin

Regulatory Protein = Calmodulin


Skeletal Muscle

Aa motor fibres

Smooth Muscle

Autonomic FIbres


Skeletal Muscle

Sequence of events from AP → muscle contraction

Depolarisation of muscle end plate via nAchR

Threshold (-50mV) reached

AP propagates

AP propagates along sarcolemma & down T-tubules

Activates L-type Ca++ ch of

T-tubles (see pic)

Flux of Ca++ intracellularly­­­↑↑↑

Ryanodine Rec of SR open = mass x60↑­ Ca++

Ca++ binds TnC

Removes inhibition of Troponin-Tropomyosin Complex

Exposes Actin binding site to myosin → commencement of cross-bridging

Myosin head pulls actin via ATP hydrolysis (ATPase) = contraction

Continues until Ca++ ↓

SERCA  pumps Ca++ back into SR → relaxation

Smooth Muscle

Wandering baseline membrane potential

(-40 to -60mV)

Depolarisation can be

  • Spontaneous
  • Ach binds muscuarinic rec (Gq) →­IP3 →SR release Ca++
  • Stretch
  • Hormonal control

Threshold reached (-35mV)

Myocyte action propogates throughout smooth m via GAP JNS→ contraction

AP opens voltage gates Ca++ ch

Ca++ enters from ECF

Opens further Ca++ from SR (insignificant)

Ca++ binds calmodulin (cytoplasm protein

Ca-Calmodulin complex activates the enzyme myosin light chain kinase (MLCK)

Initiates myosin-actin cross bridge formation → contraction by conversion of ATP to ADP

Entire muscle fibre contracts together in a corkscrew manner

Muscle Contraction continues until ATP-dependent processes actively pump Ca++ out of the cell/into SR

Sm fns for long periods, without rest, but without using a lot of energy so some sm m can retain contraction despite Ca++ removal & MLCP by cross-bridging btw actin and myosin KA LATCH BRIDGING

MLCP → dephosphorelates myosin-ATPase

  • Uncouples actin-myosin cross bridge
  • ↓intrac Ca++
  • Relaxation

Blood Flow

Skeletal Muscle

20% CO at rest

tightly regulated according to demands

Smooth Muscle

Skeletal Muscle Blood Flow

20% of CO at rest → 80% extreme exertion

1-4ml/100g/min resting → 100ml/100g/min

so there is a huge change in blood flow depending on demand:

    • Ability to maintain blood flow despite alterations in perfusion pressure
    • Myogenic mechanism
    • ­ ↑pressure → VC → ­↑resistance → ↓flow
    • (&vice versa)
    • High metabolic requirements
    • Accumulation of many VD metabolites: CO2, H+, lactate, K, Adenosine
    • Prostacyclin & NO synthesized by endothelium → VD →↑ ­flow
    • Propulsion of blood with muscle contraction
    • Symp – major regulator of vessel tone during exercise
    • a1 = VC
    • b2 = VD
    • Vasoactive hormones

Skeletal Muscle Opening of Ca++ L-Channels and SR Ca++ Ryanodine Receptor Activation

Smooth Muscle Contraction