anatomy and physiology 2211k - lecture 4. slide 2 – cytology of a muscle fiber

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