Transcript Anatomy and Physiology

Anatomy and Physiology
2211K - Lecture 4
Slide 2 – Cytology of a muscle fiber
Slide 5 – Protein filaments
Slide 4 – Actin molecule
Slide 7 – Myosin molecule
Slide 8 – Tropomyosin and troponin
Slide 9 - Tinin
Slide 10 - Nebulin
Slide 3 - Myofibrils
Slide 4 – Myofibrils II
Slide 16 – Sarcomere
Slide 12 – Energy molecules II
Slide 12 – Nucleosides
Nucleoside diphosphokinase
NTP + ADP
NDP + ATP
Nucleoside triphosphate (NTP) is a general name for all energy
molecules such as ATP, TTP, CTP, GTP, UTP
Since the conformational change of the heavy meromyosin (e.g. as an
result muscle contraction) is energized by ATP only, the remaining
energy sources (e.g. TTP, CTP, GTP, UTP) could be salvaged in an
emergency to recharge ADP
As shown above, the nucleoside triphosphate (NTP) which are the
remaining energy molecules of TTP, CTP, GTP, UTP could be utilized to
recharge ADP by transferring its high energy bond
Nucleoside diphosphokinase is the enzyme used to transfer the high
energy bone and a phosphate from NTP to ADP thereby forming ATP
Slide 13 – Creatine phosphate
Creatine Kinase
Creatine Phosphate + ADP
Creatine + ATP
Creatine phosphate is the major reserve energy source in
muscles
Creatine possesses a a high energy bond (and a phosphate)
and it is formed when the muscle is at rest
In an emergency, the high energy bond (and a phosphate) is
transferred to ADP thereby reforming a charged energy
molecule ATP
Creatine kinase is responsible for transferring the high energy
bond from creatine phosphate to ADP
Slide 14 – adenylate kinase
Adenylate Kinase
ADP + ADP
AMP + ATP
As an last ditch effort to gain energy, your body will salvage
even a spent energy molecule like Adenosine diphosphate
(ADP)
The enzyme adenylate kinase is used to transfer a phosphate
from ADP to another ADP to create a new high energy bond or a
recharged ATP
Slide 18 – Neuromuscular junction
Slide 19 – sodium and potassium concentrations
Slide 18: Polarized
Slide 18: Ionotropic and metabotropic receptor
Slide 20: Reaching threshold
Slide 20 – Spread of action potential I
Figure 17: Graphic illustration of the
formation of an action potential. Please
note that the ① pore of the ligand gated
Na+ channel (red) will open after the
binding of ACh which allows the initial
influx of Na+ and the generation of an
electric
impulse
(red
arrow).
②
Subsequently, the electric impulse will
spread down the membrane by causing the
first voltage gated Na+ channel to open
which in turn will create another electric
impulse and ③ opening another voltage
gated Na+ channel. ④ Like falling dominos,
another electric impulse will be generated
whereby causing other voltage gated Na+
channel to open
Slide 22: DHP Receptor
Figure 18: Graphic illustration of the
interactions between DHP receptor,
ryanodine receptor and calcium release
channel. ① The generated action potential
activates the DHP receptor which causes
this voltage gated Ca++ channel to open.
② Ca++ cations from the extracellular
matrix to flow into the cell. ③ The Ca++
cations bonds to ryanodine receptor
causing it to activate. ④The activated
ryanodine receptor trigger the opening of
the calcium release channel thereby
allowing the Ca++ stored within the
sarcoplasmic reticulum to be released into
the sarcoplasm
Slide 21: muscle contraction summary I
Slide 24 – Cross bride and power stroke
Slide 24: muscle contraction summary II
Figure 22: Graphic illustration of excitationcontraction coupling. ① Action potential arrives
at the neuromuscular junction which causes
AChE to be released via exocytosis. ② AChE
diffuses cross the synaptic cleft and binds with
nAChR and initiates an action potential. ③ Action
potential travels to the t-tubules and activates the
DHP receptor which in turn causes the
sarcoplasmic reticulum to release Ca++. ④ Ca++ is
released into the sarcoplasm and ⑤ binds with
troponin which in turn moves tropomyosin away
from the active site. Cross bridge is formed
between the myosin and actin myofilament and
actin-myosin cycling begins. ⑥ actin-myosin
cycling results in the shortening of the
sarcomere. The shortening of the sarcomere
causes the shortening of the myofibril. ⑦ The
shortening of the myofibril results in muscle
contraction
Slide 23: Depolarized
Slide 26: Repolarization
Slide 27: return to polarization
Slide 22 – Return to polarization and muscle relaxation summary
Figure 25: Graphic illustration of skeletal muscle
relaxation. ① Acetylcholinesterase removed
AChE which causes the nAChR to close. ② Lack
of action potential causes the voltage gated Na+
channel to close. ③ DHP receptor turns “off”
which causes the reabsorption of Ca++ by the
terminal cisternae and subsequent storage in the
sarcoplasmic reticulum. ④Removal of Ca++ from
TnC which causes troponin to return to its
original shape. Regaining its shape, troponin
moves tropomyosin back to its original
conformation. Tropomyosin covers the active site
of actin myofilament and severs the cross bridge.
⑤ Sarcomere and myofibril return to its relaxed
state. ⑥ muscle relaxation
Slide 27 - Myoglobin
Slide 31: Cellular respiration overview
Slide: Anaerobic respiration
Slide 26 – Creatine phosphate
Slide 43 – oxygen debt and lactic acid
Slide 35: aerobic and anaerobic respiration overview
Slide 36 – Types of muscle
Slide 47 – Origin, insertion and joint
Slide 48 – Flexor and extensors
Slide 49 - fasia
Slide 40 – Smooth muscle