L1i: Describe the anatomy and physiology of skeletal, smooth and cardiac muscle
Definition
Skeletal
Striated muscle tissue
Voluntary control by somatic nervous system
Cardiac
Specialized involuntary striated muscle
Smooth
Involuntary
Non-striated muscle tissue
Anatomy
Location
Skeletal
Muscle
Cardiac
Heart only
Smooth
Vessel walls
Hollow organs: stomach, intestines, uterus, bladder
Skin
Innervation
Skeletal
Aa motor fibres
Cardiac
Vagus
Cardiac sympathetic chain
Smooth
ANS
Structure
Macroscopic
Skeletal
Motor unit = nerve ending + muscle fibre
10-100mm diam fibre
Striated, ordered sarcomeres (functional unit)
Cardiac
Striated, ordered sarcomeres (functional unit)
Shorter than sk m
Syncitium – fibrous skeleton seperates atria & ventricles – allows the atria & ventricles to perform as syncytium
Smooth
No striations = looks smooth
30-200mm LENGTH →thousands of times shorter than Sk m!
Microscopic
Skeletal
Multiple parallel myofibrils
Multi nucleated
Mitochondria (aerobic & anaerobic metabolism)
SR (Ca++ storage)
Glycogen (E storage)
Myoglobin (O2 storage)
T-tubules
Cardiac
Many mitochondria AEROBIC ONLY
Myoglobin (O2 storage)
One nucleus
Rich cap network – one cap per fibre
IC disc – cell membrane – seperates each cell but allows fast communication so they can contract as a unit
Gap Jn – low resistance channel – allows depolarization to run easily btw myocytes
T-tubules – bigger & wider than T tubules of sk m – allows HUGE Ca++ influx
SR of cardiac m less well developed, relies on big Ca++ influx from T tubules
Smooth
One nucleus per cell
No striations → myosin and actin is disordered
No troponin
Calmodulin
Molecular
Skeletal
Contractile proteins = actin & myosin → Striated
Regulatory proteins = Tropomyosin & troponin
- Troponin: protein w 3 subunits
I – inhibits myosin ATPase
C- binds Ca++
T- binds Tropomysin
Tropomysin – blocks actin/myosin interaction
Cardiac
myosin → Striated
Smooth
Contractile proteins = Actin & Myosin → no order, smooth
Regulatory Protein = Calmodulin
Excitation
RMP
Skeletal
-70mV
Cardiac
-90mV
Smooth
Wandering -40 to -60mV
Source
Skeletal
NMJ
Cardiac
SA Node
Smooth
Autorhythmicity
Depolarisation can be
- Spontaneous
- Ach binds muscuarinic rec (Gq)→ ↑IP3 →SR release Ca++
- Stretch
- Hormonal control
Spread
Skeletal
Via T tubules
Cardiac
PM Cell → via conducting system
Smooth
Via Gap Jns
AP
Skeletal
Opens fast Na ch
Cardiac
Opens Fast Na and slower Ca ch → prolonged
Smooth
Na/Ca
E-C-C
Ca Release
Skeletal
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++
Cardiac
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++
Smooth
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)
Cross Bridge
Skeletal
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
Cardiac
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
Smooth
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
Relaxation
Skeletal
Continues until Ca++ ↓
SERCA pumps Ca++ back into SR → relaxation
Cardiac
Continues until Ca++ ↓
SERCA pumps Ca++ back into SR → relaxation
Smooth
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