|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.
|Properties of Skeletal muscle ||1.Velocity: Rapid.
2.Duration: Relatively long.
|Properties of Cardiac muscle ||1.Velocity: Rapid.
3.Fatigability: No fatigue (can't have the heart getting tired).|
|Properties of Smooth muscle ||1.Velocity: Slow.
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.
|Thick and Thin myofilaments ||Thick: Myosin.
|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).
|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). |