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Phys Lect 11
| Question | Answer |
|---|---|
| 3 ways of classifying muscles | 1.Control mode (Voluntary or Involuntary). 2.Histological (Straited or Smooth). 3.Anatomic (Skeletal, cardiac, smooth). |
| Important functions of smooth muscles | 1.Sphincter control. 2.Vascular tone. 3.Peristalsis. 4.Birthing contractions |
| Properties of Skeletal muscle | 1.Velocity: Rapid. 2.Duration: Relatively long. 3.Fatigability: variable. |
| Properties of Cardiac muscle | 1.Velocity: Rapid. 2.Duration: Short. 3.Fatigability: No fatigue (can't have the heart getting tired). |
| Properties of Smooth muscle | 1.Velocity: Slow. 2.Duration: Long. 3.Fatigability: No fatigue. |
| Electrical Excitation of Skeletal muscle | Comes from a motor nerve |
| Electrical Excitation of Cardia muscle | MYOGENIC: it generates its own electrical excitation which then travels through the myocardia via gap junctions. |
| Electrical Excitation of Smooth muscle | Varies, can either come from a motor nerve or move via gap junctions. |
| What ion is directly responsible for initiating contraction in all 3 muscle types? | [Ca2+]. A rise in concentration triggers a contraction. *At rest: 10^-7. *Contractoin: 10^-6 |
| Thick and Thin myofilaments | Thick: Myosin. Thin: Actin |
| Myosin Structure | Consists of: 1. 2 Globular head (important for contraction). 2.tail (flexible to allow movement for the head). |
| 2 major binding sites on the myosin head | 1.ATP binding site. 2.Actin binding site. |
| Components of the Troponin Complex? | 1.Troponin T (binds to tropomyosin). 2.Troponin I (binds to actin, inhibits Actin-myosin interaction). 3.Troponin C (responds to Ca2+). |
| A-band | Width of the myosin filaments. Includes actin overlap. |
| I-band | Actin filaments without and Myosin overlap. Contain the Z-LINES which come closer together during sarcomere shortening. |
| H-zone | Contain just the myosin without any actin overlap. Contains the M-LINE in the middle of the sarcomere |
| What happens during a contraction: A-band | STAYS THE SAME b/c the myosin filaments aren't changing in length. |
| What happens during a contraction: I-band | DECREASES, bringing the Z-lines closer together |
| What happens during a contraction: H-zone | DECREASES |
| Describe the steps of Cross-bridge cycling | 1.Myosin head is bound by ADP + Pi, ready to bind to Actin. 2.Ca2+: myosin head binds to actin. 3.Power stroke: the myosin head moves. ADP + Pi are released. 4.ATP: myosin head detaches from actin. 5.ATP hydrolysis creates a new ADP + Pi |
| [Ca2+] control which process of Cross-Bridge Cycling? | The binding of Myosin head to actin filament. **Ca+ binds to Troponin C, which then shifts tropomyosin and Troponin I so the myosin binding site on the actin filament is now exposed. |
| What happens if striated muscle is suddenly deprived of ATP? | The myosin head is stuck bound to the actin filament. (stuck contracted). **Rigormortis** |
| Myosin Light Chain Kinase | Phosphorylates the myosin head in SMOOTH muscle so that it can actively hydorlyze ATP. **It is ACTIVATED by INCREASED Ca2+** |
| Myosin Light Chain Phosphatase | Dephosphorylates the myosin head in SMOOTH muscle which prevents it from hydrolyzing ATP/contracting. |
| Ca2+ role in smooth and striated muscle contraction | 1.Smooth muscle: stimulates contraction via activating Myosin Light Chain Kinase. 2.Striated muscle: stimulates contraction via binding to Troponin C and moving tropomyosin to expose actin |
| Dystrophin | Connects the myofilaments to the cell membrane, allowing the tension/force created by smooth muscle shortening. **Problematic in MD, leads to rupturing of cell membranes and difficulty generating force due to a lack of connection |
| Muscular Dystrophy | Loss of Dystrophin, defect in cytoskeletal connection between myofilaments and muscle membrane. **Pt will present with muscle weakness, delayed coordination. Evident muscle breakdown followed by hypertrophy (as the body attempts to compensate). |