1. SKELETAL MUSCLE
1. SKELETAL MUSCLE Excitation Contraction Coupling: contraction relies on excitation (transmission of neural impulse along sarcolemma and t-tubules) T-tubules: sarcollema folds in so excitation can reach inside of muscle. T-tubule is OUTSIDE muscle fibre ECC STEPS: 1. Action potential crosses muscle membrane 2. DHPR (voltage sensitive receptor) activated 3. RyR opens when DHPR is activated because they are touching (allows action potential inside muscle) 4. Calcium kept in S.R flows out when RyR opens (very little calcium in actual muscle cell, most kept in S.R. Held in place by calsequestrin. 5. Cross bridge cycling = muscle shortening (contraction) 6. Ca removal = muscle relaxation 7. SERCA = calcium back into S.R Ca2+ REGULATORY SYSTEM: Relaxed: -
Tropomyosin prevents actin (thin filament) and myosin head coming together Troponin holds tropomyosin in place. (T=bound to tropomyosin, C=binds to calcium, I=inhibitory)
Increased calcium: -
Calcium binds to troponin C Myosin head can bind to actin Amount of force controlled by number of binding sites exposed
RELAXATION: SERCA: Sarcoplasmic Endoplasmic Reticulum pump -
Calcium comes off troponin C 2 calciums bind to SERCA Hydrolysis of ATP to ADP + Pi 1 ATP = 2 calciums back into S.R
SLIDING FILAMENT THEORY: -
A band (myosin, thick filament) unchanged I band and H band reduced length (actin filaments, thin) – book shelf and rope example
CROSS BRIDGE CYCLE: -
Myosin head activated by hydrolysis of ATP Cross bridge formation: myosin head and actin binding
-
Power stroke: ADP released from myosin head, cross bridge moves because myosin head position is changed Cross bridge detachment: ATP binds to myosin, bond weakens Reactivation of myosin head: hydrolysis of ATP so ADP and Pi can bind Cross bridges cycle so that there is always something attached – tug of war example Thin microfilaments (actin) pulled together = contraction
CRITICAL THINKING EXAMPLES: AcH remaining in neuromuscular junction would mean the muscle would stay contracted DHPR-RyR chronically open: too much contraction, overheating (anaesthetic) DHPR-RyR difficult to open: calcium release channels not open = no contraction Slow hydrolysis of ATP on myosin = less cross bridging, therefore less force SERCA working too slowly: too much calcium, degradation Shorter cross bridges = less force produced because there is less available distance to shorten
Tropomyosin prevents actin (thin filament) and myosin head coming together Troponin holds tropomyosin in place. (T=bound to tropomyosin, C=binds to calcium, I=inhibitory)
Increased calcium: -
Calcium binds to troponin C Myosin head can bind to actin Amount of force controlled by number of binding sites exposed
RELAXATION: SERCA: Sarcoplasmic Endoplasmic Reticulum pump -
Calcium comes off troponin C 2 calciums bind to SERCA Hydrolysis of ATP to ADP + Pi 1 ATP = 2 calciums back into S.R
SLIDING FILAMENT THEORY: -
A band (myosin, thick filament) unchanged I band and H band reduced length (actin filaments, thin) – book shelf and rope example
CROSS BRIDGE CYCLE: -
Myosin head activated by hydrolysis of ATP Cross bridge formation: myosin head and actin binding
-
Power stroke: ADP released from myosin head, cross bridge moves because myosin head position is changed Cross bridge detachment: ATP binds to myosin, bond weakens Reactivation of myosin head: hydrolysis of ATP so ADP and Pi can bind Cross bridges cycle so that there is always something attached – tug of war example Thin microfilaments (actin) pulled together = contraction
CRITICAL THINKING EXAMPLES: AcH remaining in neuromuscular junction would mean the muscle would stay contracted DHPR-RyR chronically open: too much contraction, overheating (anaesthetic) DHPR-RyR difficult to open: calcium release channels not open = no contraction Slow hydrolysis of ATP on myosin = less cross bridging, therefore less force SERCA working too slowly: too much calcium, degradation Shorter cross bridges = less force produced because there is less available distance to shorten
