anatomy and physiology 2211k - lecture 4. slide 2 – cytology of a muscle fiber
TRANSCRIPT
Anatomy and PhysiologyAnatomy and Physiology
2211K - Lecture 42211K - 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
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
Nucleoside diphosphokinase
Slide 13 – Creatine phosphate
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
Creatine Kinase
Slide 14 – 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
Adenylate Kinase
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 pore of the ligand gated ①Na+ 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). ②Subsequently, 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 opening another voltage ③gated Na+ channel. Like falling dominos, ④another 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. The generated action potential ①activates the DHP receptor which causes this voltage gated Ca++ channel to open. ②Ca++ cations from the extracellular matrix to flow into the cell. The Ca③ ++ cations bonds to ryanodine receptor causing it to activate. The activated ryanodine ④receptor 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 excitation-contraction coupling. Action potential arrives ①at the neuromuscular junction which causes AChE to be released via exocytosis. AChE ②diffuses cross the synaptic cleft and binds with nAChR and initiates an action potential. Action ③potential travels to the t-tubules and activates the DHP receptor which in turn causes the sarcoplasmic reticulum to release Ca++. Ca④ ++ is released into the sarcoplasm and binds with ⑤troponin 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. actin-myosin ⑥cycling results in the shortening of the sarcomere. The shortening of the sarcomere causes the shortening of the myofibril. The ⑦shortening 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. Acetylcholinesterase removed ①AChE which causes the nAChR to close. Lack ②of action potential causes the voltage gated Na+ channel to close. DHP receptor turns “off” ③which causes the reabsorption of Ca++ by the terminal cisternae and subsequent storage in the sarcoplasmic reticulum. Removal of Ca④ ++ 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.
Sarcomere and myofibril return to its relaxed ⑤state. muscle relaxation ⑥
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