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Muscle and their types
Molecular Mechanism of Contraction
Mechanism of Single Fiber Contraction
Presentation Topics:
01:
Muscle
A band or bundle of fibrous tissue in a human or animal body that has the ability to contract, producing movement in or maintaining the position of parts of the body.
There are about 600 muscles in the human body. The main three types of muscles are:
Skeletal Muscle
Smooth Muscle
Cardiac Muscle
Skeletal Muscle
Skeletal muscles comprise 30 to 40% of your total body mass.
Microscopic Structure of Skeletal Muscle
Muscle Fibers: Long, multinucleated cells forming the basic unit.
Myofibrils: Thread-like structures within fibers, housing sarcomeres.
Sarcomeres: Contractile units composed of actin and myosin filaments, delineated by Z-lines.
Connective Tissue Layers: Endomysium around fibers, perimysium around fascicles, and
epimysium enveloping the entire muscle.
Vascularization and Innervation: Blood vessels and nerves traverse connective tissue layers, supplying nutrients and nerve signals.
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Molecular Mechanism of Contraction:
**Molecular Mechanism of Contraction**
1. **Neuromuscular Junction Activation:**
- Release of acetylcholine (ACh) from motor neurons.
- Binding of ACh to receptors on the sarcolemma.
2. **Action Potential Initiation:**
- Depolarization of sarcolemma by ACh binding.
- Propagation of action potential along T-tubules.
3. **Calcium Release:**
- Action potential triggers calcium release from sarcoplasmic reticulum.
- Calcium ions flood into the sarcoplasm.
4. **Troponin Activation:**
- Calcium binds to troponin on the actin filament.
- Conformational change in troponin-tropomyosin complex.
5. **Cross-Bridge Formation:**
- Myosin heads bind to exposed actin binding sites.
- Formation of cross-bridges between actin and myosin.
Molecular Mechanism of Contraction:
6. **Power Stroke:**
- ATP hydrolysis energizes myosin heads.
- Myosin heads pivot, pulling actin filaments inward.
7. **ADP and Pi Release:**
- Release of ADP and inorganic phosphate (Pi).
- Myosin remains attached to actin.
8. **ATP Binding and Detachment:**
- ATP binds to myosin heads, causing detachment from actin.
- ATP hydrolysis resets myosin heads for next cycle.
9. **Relaxation:**
- Removal of calcium ions from sarcoplasm.
- Troponin-tropomyosin complex covers actin binding sites.
- Muscle relaxation occurs.
Mechanism of Single Fiber Contraction
The mechanism of single fiber contraction in skeletal muscle involves a series of intricate biochemical and mechanical events:
Neuromuscular Junction Activation: Stimulation from a motor neuron causes acetylcholine release at the neuromuscular junction.
Action Potential Propagation: Acetylcholine triggers an action potential in the muscle fiber membrane (sarcolemma).
Calcium Release: Action potential propagation leads to calcium release from the sarcoplasmic reticulum.
Troponin Activation: Calcium binds to troponin, inducing a conformational change in the troponin-tropomyosin complex.
Actin-Myosin Interaction: Exposed binding sites on actin allow myosin heads to bind, forming cross-bridges.
Power Stroke: ATP hydrolysis energizes myosin heads, causing them to pivot and pull actin filaments toward the center of the sarcomere.
ADP and Pi Release: ADP and inorganic phosphate (Pi) are released, but myosin remains attached to actin.
ATP Binding and Detachment: ATP binds to myosin, causing detachment from actin.
Myosin Head Reset: ATP hydrolysis resets myosin heads for another cycle.
Relaxation: Calcium is actively transported back into the sarcoplasmic reticulum, allowing for troponin-tropomyosin complex to cover binding sites, leading to muscle relaxation.
Cardiac Muscle
Structure:
Intercalated Discs: Intercalated discs are specialized regions that join adjacent cardiomyocytes end-to-end. These discs contain three main structures:
Sarcomeres: Cardiomyocytes contain sarcomeres, which are the basic contractile units of muscle fibers
Mitochondria: Mitochondria are responsible for producing the ATP needed to fuel muscle contractions.
T-tubules: Cardiac muscle cells have invaginations of the sarcolemma (cell membrane) called T-tubules, which penetrate into the cell's interior.
Sarcoplasmic Reticulum (SR): The sarcoplasmic reticulum is a specialized form of endoplasmic reticulum found in muscle cells. It stores and releases calcium ions (Ca2+), which are essential for muscle contraction. Calcium release from the SR triggers the sliding of actin and myosin filaments during contraction.
Molecular mechanism of Contraction
Calcium Ion Influx:
Action potentials propagate through cardiac muscle cells, leading to calcium influx through voltage-gated calcium channels.
Calcium-induced Calcium Release:
Influx of calcium triggers additional release of calcium from the sarcoplasmic reticulum via ryanodine receptors.
Troponin-Calcium Binding:
Calcium binds to troponin C on the thin filaments, causing a conformational change in the troponin-tropomyosin complex.
Actin-Myosin Interaction:
Exposed binding sites on actin allow myosin heads to bind, forming cross-bridges.
Power Stroke and Contraction:
ATP hydrolysis energizes myosin heads, leading to the power stroke and pulling of actin filaments.
ADP and Pi Release:
ADP and inorganic phosphate (Pi) are released, but myosin remains attached to actin.
ATP Binding and Detachment:
ATP binds to myosin, causing detachment from actin.
Relaxation:
Calcium is actively transported back into the sarcoplasmic reticulum by calcium pumps.
Troponin-tropomyosin complex covers actin binding sites, leading to muscle relaxation.
Single Fiber Conntraction Mechanism
Single Fiber Mechanism of Contraction in Cardiac Muscle
Action Potential Initiation:
Action potentials are initiated in cardiac muscle cells by pacemaker cells in the sinoatrial node.
Calcium Influx:
Action potentials propagate through T-tubules, leading to calcium influx through L-type calcium channels.
Calcium-induced Calcium Release:
Calcium influx triggers further release of calcium from the sarcoplasmic reticulum via ryanodine receptors.
Troponin-Calcium Binding:
Calcium binds to troponin C, initiating a conformational change in the troponin-tropomyosin complex.
Cross-Bridge Formation:
Exposed binding sites on actin allow myosin heads to bind, forming cross-bridges.
Power Stroke and Contraction:
ATP hydrolysis energizes myosin heads, leading to power stroke and actin filament pulling.
Relaxation:
Calcium is actively transported back into the sarcoplasmic reticulum by calcium pumps, promoting muscle relaxation. Troponin-tropomyosin complex covers actin binding sites, leading to muscle relaxation.
Smooth muscle
Structure of Smooth Muscle
Molecular and Single Fiber Contraction Mechanism of Smooth Muscle
Action Potential Generation:
Nervous or hormonal signals trigger action potentials in smooth muscle cells.
Calcium Influx:
Action potentials cause calcium influx through voltage-gated channels or release from intracellular stores.
Calcium-Calmodulin Complex Formation:
Calcium binds to calmodulin, activating MLCK.
MLC Phosphorylation:
MLCK phosphorylates MLC, initiating cross-bridge formation.
Cross-Bridge Cycling:
Phosphorylated myosin heads interact with actin, generating force and shortening the muscle fiber.
Relaxation:
Removal of calcium from the cytoplasm leads to dephosphorylation of MLC by MLCP, promoting relaxation.
Calcium Ion Influx:
Calcium ions enter the cytoplasm from extracellular sources or intracellular stores.
Calcium-Calmodulin Complex Formation:
Calcium binds to calmodulin, forming an active complex.
Activation of Myosin Light Chain Kinase (MLCK):
Calcium-calmodulin complex activates MLCK enzyme.
Phosphorylation of Myosin Light Chains (MLC):
MLCK phosphorylates MLC, activating myosin ATPase.
Cross-Bridge Formation:
Phosphorylated myosin heads bind to actin, forming cross-bridges.
Power Stroke and Contraction:
ATP hydrolysis leads to power stroke, pulling actin filaments.
Relaxation:
Decrease in cytoplasmic calcium leads to dephosphorylation of MLC by myosin light chain phosphatase (MLCP).