Muscle contraction Flashcards
There are three types of muscle:
skeletal, cardiac, smooth
Skeletal muscle is controlled by the somatic nervous system. Cardiac and smooth are influenced by the autonomic nervous system
cardiac and smooth are striated - Striation is due to organisation of contractile proteins in the cell
myofibrils
Each muscle cell contains many parallel myofibrils
Skeletal muscle activity
Controlled by somatic motor neurons located in spinal cord & brainstem. “Motor unit” = one motor neuron plus the muscle cells it targets
The neuromuscular junction
- A type of chemical synapse.
- Ach acts on nicotinic receptors to produce an “end plate potential”
- Voltage-gated Na+ channels start in the adjacent membrane.
- The “end plate potential” always triggers an AP in the muscle cell.
Neuromuscular junction process
acetylcholine released by axon of motor neuron crosses cleft and binds to receptors/channels on motor end plate > enters T tubule > triggers Ca++ release from sarcoplasmic reticulum into skeletal muscle cell
Sarcoplasmic reticulum
Sarcoplasmic reticulum sits next to myofibrils
The sarcomere
The sarcomere is the basic contractile unit in skeletal muscle
thin myofilament - Actin
Thick myofilament - Myosin
Ca++ triggers actin/myosin interaction, actin filaments slide over thick filaments towards centre and sarcomere shortens
- without ATP can’t have contraction
Calcium ions triggering actin and myosin interaction resulting in POWER STROKE.
• The sequence of events that results in the excitation contraction coupling is:
- Action potential enters the T-tubule
- AP then activates the sarcoplasmic reticulum to release Ca2+
- Ca2+ binds to troponin
- Troponin-Ca2+ complex pulls the tropomyosin exposing the binding sites on actin
- Myosin heads bind to actin and with the release of Pi from ADP, Myosin head bends resulting in the power stroke
- New ATP binds to Myosin head releasing the bond between Myosin and Actin
- Ca2+ is pumped back into the SR
The key element of actin/myosin interaction is “crossbridge cycling”
actin molecules in thin myofilament and myosin cross bridge > binding Myosin cross bridge to actin molecule > power stroke cross bridge bends, pulling thin myofilament inwards
- Requires constant supply of ATP for muscle contraction
- 6 actin fillaments, 6 myosin fillaments
Excitation-contraction coupling in skeletal muscle
• Action potential in motor neuron
• Release of ACh at the neuromuscular junction
• ACh action at nicotinic receptors triggers an
end-plate potential
• AP initiated in skeletal muscle membrane
• AP enters T-tubules
• Ca++ release from sarcoplasmic reticulum • Ca++ triggers crossbridge cycling
• Sarcomeres shorten
• Muscle contracts
Cellular structure affects skeletal muscle function
At resting muscle length, no relationship btwn actin or pyosin (100%)
at 170%, full lengthening
at 60%, full shortening
golgi tendon organ
golgi tendon organ acts as relief valve when to much tension is developed on muscles, prevents damage from happening
* If muscle stretched > fires a lot of AP
knee jerk reflex
reflex stimuatles in the spinal cord > the motor neurons to the extensor muscle > inhibits the motor neurons to the flexor muscles
Production of ATP in skeletal muscle
get from brake down from glucose via glycolysis - 2
- 36 from oxidative phosphorylaction and 1 creatine phosphate
slow twitch muscles
The ATP required for slow-twitch fiber contraction is generated through aerobic respiration (glycolysis and Krebs cycle