SKELETAL MUSCLE CONTRACTION & RELAXATION -MECHANISM
CONTRACTION PROCESS:
- Muscle contraction/shortening occurs due to sliding of filaments (actin on myosin).
- Basic contractile unit of muscle – Sarcomere.
- Four types involved:
– Actin, Myosin, Tropomyosin, & Troponin.
1. Myosin:
- Protein with thick filaments.
- Myosin type in skeletal muscle – Myosin-II.
- More concentrated in H-zone. (Central part of A-band).
Functions:
- Participates in contractile mechanism.
- Acts as an ATPase.
2. Actin:
- Major protein with thin filaments.
- Actin which slides over myosin during contraction.
- Absent in H-zone.
3. Tropomyosin:
- Thin filament protein.
- Covers active sites (myosin binding sites) on actin.
- Increased sarcoplasmic Ca2+ concentration → Uncovers/covers active sites of actin & allows contraction.
– Hence, cross-bridge cycling is switched off/on.
4. Troponin:
- Thin filament protein.
- Ca2+ binding protein.
- Mediates Ca2+ regulatory action on Tropomyosin.
Additional structural proteins in skeletal muscles:
1. Actinin
- Binds actin to Z-lines.
2. Titin –
- Largest known protein.
- Connects Z-lines to M-lines.
- Act as a framework holding myosin & actin filaments in place.
– Ensures sarcomeric contractile machinery works smoothly.
- Also responsible for passive muscle stiffness.
- Limits sarcomere’s range of motion in tension.
3. Desmin
- Adds structures to Z lines.
- By binding Z-lines to plasma membrane.
- Cytoplasmic/sarcoplasmic Ca2+ concentration.
- Results in Ca2+ ions binds to troponin-C.
- Troponin – Ca2+complex induces → Changes in Troponin-I & Troponin-T.
– Inturn shifts tropomyosin away from active sites of actin.
– Resulting in uncovering/exposure of active binding sites on actin filament.
– Thus contracts muscle.
2. Decreased sarcoplasmic Ca2+ concentration:
Events following:
- Results in Ca2+ dissociates from troponin-C.
- Tropomyosin slides back on actin filament covering active sites.
- Results in muscle relaxation.
- Process by initiation of contraction by excitation/depolarization of muscle fiber.
- Caused by Ca2+ ions.
MECHANISM OF MUSCLE CONTRACTION:
Discharge in Aα motor neuron.
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Release of acetylcholine at NM junction from presynaptic vesicles.
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Binding of acetylcholine to nicotinic(Nm) Ach receptors.
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Opens Na+ channels in motor end plate.
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End plate potential generated.
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Action potential generation on sarcolemma adjacent to Nm junction.
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AP spreads in muscle fibers in both directions.
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In-ward depolarization spread along T-tubules
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Interaction of Di-Hydropyridine (DHPR) & Ryanodine (RyR) receptor in terminal cisterns of sarcoplasmic reticulum.
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Ca2+ ion release from sarcoplasmic terminal cisterns via Ryanodine receptor.
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Increased sarcoplasmic Ca2+ concentration.
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Binds with troponin C & Ca2+.
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Lateral movement of tropomyosin uncovering active sites of actin.
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Cross-linkage of myosin with actin → Muscle contracts.
- First event during muscle contraction after increased cytoplasmic Ca2+ concentration is binding troponin C to Ca2+.
– This triggers tropomyosin sliding away from active sites of actin.
– Mysoin cross-links with actin causing muscle contraction.
IMPORTANT EVENTS DURING MUSCLE CONTRACTION:
1. Changes in muscle fibers during contraction:
- Z lines come closer → Shortens sarcomere.
- H-band disappears.
- I band width decreases.
- Unchanged A bandwidth.
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Results in very high Ca2+ concentration in terminal cisterns & very low in sarcoplasm.
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Tropomyosin covers active sites of actin.
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Myosin-actin cross-linkage ceased → Muscle relaxation.
ROLE OF ATP:
ATP has three roles in muscle contraction & relaxation:
- Provides energy for power stroke of myosin head.
- Dissociates myosin head from actin filament.
– Only under low sarcoplasmic Ca2+ concentration.
- Pumps out Ca2+ from sarcoplasm into terminal cisterns of sarcoplasmic reticulum.
– Thus causing muscle relaxation.
During muscle-relaxation cycle-
- ATP with high Ca2+ in cytoplasm → Ongoing cross-bridge cycle & muscle contraction.
- ATP with low Ca2+ in cytoplasm → Interruption of cross-bridge cycle & muscle relaxation.
- ATP depletion results in –
– Rigor mortis – Muscle rigidity after death.
– Muscle fatigue during severe exercise resulting in a contracted state.
Exam Important
- Basic contractile unit of muscle – Sarcomere.
- Four muscle proteins are Actin, Myosin, Tropomyosin, & Troponin.
- Myosin are thick filament protein.
– Myosin-II – Specific type in skeletal muscle.
– More concentrated in H-zone (Central part of A-band).
– Acts as an ATPase.
- Actin are major protein with thin filaments.
– Slides over myosin during contraction.
– Absent in H-zone.
- Tropomyosin is thin filament protein.
– Covers active myosin binding sites on actin.
- Troponin is thin filamented Ca2+ binding protein.
- Titin connects Z-lines to M-lines.
– Act as framework holding myosin & actin filaments in place.
- Cytoplasmic/sarcoplasmic Ca2+ levels regulate muscular contraction & relaxation mechanisms.
- Increased sarcoplasmic Ca2+ concentration results in Ca2+ binding to troponin-C.
– Troponin – Ca2+complex further induces changes in Troponin-I & Troponin-T for muscle contraction.
↓
Release of acetylcholine at NM junction from presynaptic vesicles.
↓
Binding of acetylcholine to nicotinic (Nm) Ach receptors.
↓
Interaction of Di-Hydropyridine (DHPR) & Ryanodine (RyR) receptor in terminal cisterns of sarcoplasmic reticulum.
↓
Ca2+ ion release from sarcoplasmic terminal cisterns through Ryanodine receptor.
↓
Increased sarcoplasmic Ca2+ concentration.
↓
Binds with troponin C & Ca2+.
↓
Lateral movement of tropomyosin with uncovering of active sites of actin.
↓
Cross-linkage of myosin with actin & Muscle contracts.
- Z lines come closer → Shortens sarcomere.
- H-band disappears.
- I bandwidth decreases.
- First event during muscle contraction is troponin C binding to Ca2+.
– In turn, triggers tropomyosin sliding away from active sites of actin.
– Myosin cross-links with actin contracting muscle.
Results in very high Ca2+ concentration in terminal cisterns & very low in sarcoplasm.
↓
↓
Cessation of interaction between myosin & actin with resultant muscle relaxation.
- ATP provides energy for power stroke of myosin head.
- Dissociates myosin head from actin filament.
– Only under low Ca2+ sarcoplasmic concentration.
- Pumps out sarcoplasmic Ca2+ into terminal cisterns of sarcoplasmic reticulum, causing muscle relaxation.
- ATP depletion results in,
– Rigor mortis – Muscle rigidity after death.
– Muscle fatigue during severe exercise resulting in a contracted state.
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